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At least 199 records · Page 11Linked to original sources
PubMed1998

Central nervous system vasculitis.

Central nervous system vasculitis occurs in a variety of clinical settings. Some exhibit a distinct age preference; others a tissue tropism. Most frequently encountered are giant cell arteritis (temporal arteritis) and vasculitis secondary to infections. The central nervous system may be involved in the antineutrophil cytoplasmic antibody-associated systemic vasculitides and occasionally neurologic abnormalities appear as a presenting manifestation of disease. Isolated angiitis of the central nervous system, a rare form of vasculitis that is restricted to the central nervous system, must be distinguished from other causes of central nervous system inflammation and from noninflammatory vascular disease. We are learning a great deal about the cellular mechanisms of vascular inflammation in general. Some manifestations of the clinical disease result from histologic features of the infiltrate and the size of affected vessel. However, the local consequences of inflammation, such as increased coagulation and altered vasomotor tone, as well as the systemic consequences, such as activation of the central noradrenergic systems, trigeminovascular system, and hypothalamic pituitary adrenal axis, contribute both to pathogenesis of disease and to recovery.

Behcet Syndrome↗
PubMed2001

[Calcium ions and the nervous system plasticity].

The nervous system is different from all other systems of the organism by extreme flexibility of the structural and functional properties of its elements. This unique feature of the nervous system can be best described as plasticity in a broad sense of the word. All forms of plastic changes in the nervous system functioning have common basic mechanisms, the changes at the free Ca2+ cytosol ions being the most important one. These "calcium signals" trigger an extremely complicated intracellular machinery capable of controlling the structural and functional properties of the nervous system during the whole life span. This review summarises data on the intracellular Ca2+ ions mechanisms controlling the developmental plasticity of neuronal elements, synaptic plasticity of the mature nervous system, and the decline of plastic capabilities with ageing.

Aging↗
PubMed2002

Nervous system Lyme disease.

Nervous system involvement in Lyme borreliosis is a much-feared, often-misunderstood disorder. Both the peripheral and central nervous systems may be involved, typically in a multifocal, patchy fashion, perhaps suggesting a vasocentric mechanism. Clinical manifestations vary widely, depending on the site and severity of involvement. Although neurologic manifestations observed in Europe differ somewhat from those reported in the United States, there are also striking similarities, permitting some generalization of information obtained in each population. In general, diagnosis of neurologic disease requires objective evidence of nervous system damage, and must be differentiated from both psychiatric disorders and metabolic encephalopathies, both of which typically occur in the absence of significant neurologic damage or infection. Laboratory confirmation of nervous system involvement by Borrelia burgdorferi has limitations. However, neurophysiologic testing of the peripheral nervous system, imaging of the neuraxis, and examination of the cerebrospinal fluid can all be informative. In contrast, to date functional brain imaging has been of limited specificity. Treatment with one of several straightforward antimicrobial regimens, typically 2-4 weeks in duration, generally results in microbiologic cure. Although some symptoms may persist after this, the data do not suggest that these are responsive to further antimicrobial therapy.

Europe↗
PubMed1984

[The central nervous system, regulation of blood pressure and hypertension. Recent advances in the role of the central nervous system in the regulation of blood pressure].

Evidence for a contribution of the central nervous system to the development and maintenance of high blood pressure disease is accumulating. Increased activity of the sympathetic nervous system has been demonstrated experimentally and clinically. Centrally acting drugs such as a-methyldopa, clonidine or reserpine effectively lower blood pressure. CNS dysregulation, as seen by alterations in neurotransmitter concentrations or baroreceptor reflex function, have been detected in early stages of hypertension. In animal experiments renal hypertension could be prevented by central chemical sympathectomy. Finally, psychosocial stress can induce sustained hypertension and a relationship between personality pattern, conflict behaviour and high blood pressure has been established.

Animals↗
PubMed1990

[In search of the lymphatic system of the central nervous system].

Lymphatic flow in the brains and lymphatic vessels in the meninges are recognized through the intra-cerebral injection of a dye specific to the lymphatic system. The confluence of these two components can only be at the level of the cerebro spinal fluid (CSF), which lends support to the hypothesis that the CSF itself constitutes the lymph of the nervous system. The authors report the results of a study based on a necropsic investigation and an experimental animal model, contributing new facts in favor of this hypothesis. For a certain number of inflammatory diseases of the central nervous system (CNS) when the initial phase is still limited to the brain or to the spinal chord tissues, it is usually asymptomatic; only when it reaches the meninges, that clinical symptoms be seen: this can be explained by the presence of such lymphatic circulatory system. Stasis of the cerebral lymphatic circulation, should be regarded as a new etiologic factor in the onset of brain oedemas. This concept, already taken into account by some investigators, deserves consideration in the study of most CNS diseases.

Animals↗
PubMed1985

Hydergine: interaction with the neurotransmitter systems in the central nervous system.

Hydergine (co-dergocrine, ergoloid mesylates, dihydroergotoxine) is an ergot preparation which has been shown to be of value in the treatment of senile mental impairment. Results from biochemical in vitro investigations suggest that Hydergine interacts directly with subtypes of alpha-adrenoceptors, dopamine and serotonin receptors. For instance, in slices of rat cerebral cortex, it blocked noradrenaline-induced increase of cyclic AMP content and facilitated electrically evoked noradrenaline release which is consistent with antagonistic properties at postsynaptic alpha 1- and presynaptic alpha 2-adrenoceptors. Furthermore, Hydergine had mixed agonist/antagonist properties at postsynaptic D1 receptors mediating stimulation of adenylate cyclase, and at pre- and postsynaptic D2 receptors mediating inhibition of evoked dopamine and acetylcholine release in the rat striatum, respectively. Hydergine had also mixed agonist/antagonist properties at the serotonin-sensitive adenylate cyclase in the rat hippocampus and the presynaptic serotonin autoreceptors present on nerve terminals in the rat cortex. Based on these in vitro data, it is suggested that Hydergine influences central monoaminergic systems in a dualistic manner. On the one hand, it can compensate for a transmitter deficit in dopaminergic and serotoninergic systems, but at the same time, counteract a possible hyperactivity in the same transmitter systems. The noradrenergic systems may be affected in a similar way but by a different mechanism. In this latter system, Hydergine increased evoked noradrenaline release by blocking presynaptic alpha-adrenergic autoreceptors, but by a simultaneous blockade of postsynaptic alpha 1-adrenoceptors sets a ceiling effect to the noradrenergic stimulation. Thus, Hydergine might be able to counteract and prevent disturbances in the interplay between monoaminergic and other transmitter systems in the central nervous system. It is proposed that these multiple effects of Hydergine are in part responsible for its beneficial effects in senile mental impairment.

Aged↗
PubMed2006

Anatomy of the Hesse photoreceptor cell axonal system in the central nervous system of amphioxus.

The present study reports the organization of the Hesse cell axonal system in the central nervous system of the amphioxus, with the use of a polyclonal antiserum raised against lamprey gonadotropin-releasing hormone-I (GnRH-I). In the spinal cord, the rhabdomeric photoreceptor cells of the bicellular organs were well labeled with this antibody. These cells sent smooth, straight, lateral processes that bent and became beaded as they passed ventrally and crossed to the contralateral side of the cord. There, the processes of several cells aggregated to give rise to a longitudinal fiber bundle. Beaded collaterals of these processes were directed to ventral neuropil and did not appear to contact giant Rohde cell axons. The crossed projections of the Hesse photoreceptors are compared with those of vertebrate retinal ganglion cells. Other antisera raised against GnRH weakly labeled rhabdomeric photoreceptors located dorsally in the brain, the Joseph cells. The finding that GnRH antibodies label amphioxus photoreceptor cells and axons is not definitive proof that the photoreceptors contain GnRH. Regardless of whether the antibody recognizes amphioxus GnRH, which has not yet been identified by structure, the antibody has revealed the processes of the Hesse photoreceptor cells.

Animals↗
PubMed1981

Similarity of neurofilament proteins from different parts of the rabbit nervous system.

In the nervous system, the various populations of neurons perform a large spectrum of functions. Although neurofilaments are a major constituent of the different neurons, the neurofilament protein composition and the expression of the genes specifying these proteins may not be the same throughout the entire nervous system. To investigate these two aspects of the biology of neurofilaments, we have prepared neurofilament-rich fractions from different regions of the nervous system of strains of rabbits known to present a genetically determined polymorphism involving one of the neurofilament polypeptides (P200). Filaments were isolated from brain, spinal cord, sciatic, optic and trigeminal nerves, and lumbar ventral and dorsal roots by a procedure not involving axonal flotation and yielding material suitable for comparative analysis within a single animal. The filaments were compared for their variability as a function of the region from which they were prepared. For any given animal, the neurofilament peptides migrate to identical positions on SDS-gel electropherograms. Whatever allele of P200 is expressed in filaments from one region, the same allele is also expressed in all of the other filament preparations from that animal. On two-dimensional analysis isomorphs of the P68 neurofilament protein are not present in the same amounts in different regions of the nervous system. These results indicate that, although it seems that the gene for the P200 neurofilament protein is expressed uniformly throughout the nervous system, there may be some topographic specificity in the distribution of the other constituent proteins of neurofilaments.

Animals↗
PubMed1990

Pressure wave injuries to the nervous system caused by high-energy missile extremity impact: Part II. Distant effects on the central nervous system--a light and electron microscopic study on pigs.

The aim of the present study was to investigate if distant effects could be detected within the central nervous system after impact of a high-energy missile in the left thigh of young pigs. Pressure transducers implanted in various parts of the body of the animal, including the brain, recorded a short-lasting burst of oscillating pressure waves with high frequencies and large amplitudes, traversing the body tissue with a velocity of about that of sound in water (1,460 m/s). The distance between the point of impact and the brain and cervical spinal cord is in the range of 0.5 m. Macroscopic examination revealed that there was no gross brain tissue disruption or visible blood-brain barrier dysfunction. Light microscopic examination demonstrated myelin invaginations in the largest axons and shrinkage of axoplasm. Electron microscopic examination revealed a reduction in the number of microtubules, especially in the larger axons in the brainstem. Disintegration of Nissl substance, i.e., chromatolysis, was noticed after 48 hr in many Purkinje nerve cells in the cerebellum, concomitantly with the appearance of an increased frequency of association between lamellar bodies and mitochondria. Changes could also be observed in the cervical spinal cord and, at reduced frequency and extent, in the optic nerve and in other parts of the brain. These effects were evident within a few minutes after the trauma and persisted even 48 hr after the extremity injury. It is concluded that distant effects, likely to be caused by the oscillating high-frequency pressure waves, appear in the central nervous system after a high-energy missile extremity impact.

Abdomen↗
PubMed2005

At the interface of the immune system and the nervous system: how neuroinflammation modulates the fate of neural progenitors in vivo.

Neural stem and progenitor cells express a variety of receptors that enable them to sense and react to signals emanating from physiological and pathophysiological conditions in the brain as well as elsewhere in the body. Many of these receptors and were first described in investigations of the immune system, particularly with respect to hematopoietic stem cells. This emerging view of neurobiology has two major implications. First, many phenomena known from the hematopoietic system may actually be generalizable to stem cells from many organ systems, reflecting the cells' progenitor-mediated regenerative potential. Second, regenerative interfaces may exist between diverse organ systems; populations of cells of neuroectodermal and hematopoietic origin may interact to play a crucial role in normal brain physiology, pathology, and repair. An understanding of the origins of signals and the neural progenitors' responses might lead to the development of effective therapeutic strategies to counterbalance acute and chronic neurodegenerative processes. Such strategies may include modifying and modulating cells with regenerative potential in subtle ways. For example, stem cells might be able to detect pathology-associated signals and be used as "interpreters" to mediate drug and other therapeutic interventions. This review has focused on the role of inflammation in brain repair. We propose that resident astroglia and blood-born cells both contribute to an inflammatory signature that is unique to each kind of neuronal degeneration or injury. These cells play a key role in coordinating the neural progenitor cell response to brain injury by exerting direct and indirect environmentally mediated influence on neural progenitor cells. We suggest that investigations of the neural progenitor-immunologic interface will provide valuable data related to the mechanisms by which endogenous and exogenous neural progenitor cells react to brain pathology, ultimately aiding in the design of more effective therapeutic applications of stem cell biology. Such improvements will include: (1) ascertaining the proper timing for implanting exogenous neural progenitor cells in relation to the administration of anti-inflammatory agents; (2) identifying what types of molecules might be administered during injury to enhance the mobilization and differentiation of endogenous and exogenous neural progenitor cells while also inhibiting the detrimental aspects of the inflammatory reaction; (3) divining clues as to which molecules may be required to change the lesioned environment in order to invite the homing of reparative neural progenitor cells.

Animals↗
PubMed1982

Cytofluorescence localization of adriamycin in the nervous system. II. Distribution of the drug in the somatic and autonomic peripheral nervous systems of normal adult mice after intravenous injection.

By a fluorescence-microscopic technique, the distribution of the antineoplastic glycoside adriamycin (doxorubicin) was studied in the peripheral nervous system (PNS) of normal adult mice after i.v. injection. Doses comparable to those used in patients for treatment of malignant diseases were used. The orange-red fluorescence of the drug was observed in dorsal root ganglia, in the trigeminal ganglia, and in the superior cervical sympathetic ganglia where it was preferentially accumulated in the nuclei of satellite cells. This nuclear labeling was a very quick process which occurred in the superior cervical ganglion within 15 s after the injection. Adriamycin-fluorescent nuclei were also observed in the suprarenal medulla. Fluorescent nuclei were present within the pre- and postganglionic sympathetic nerve trunks close to the superior cervical ganglion but not in the endoneurium of the trigeminal and the sciatic nerves or in the spinal nerve roots. In such structures labeled cells appeared in the connective tissue sheaths covering the nerves and the roots. No adriamycin-induced fluorescence was detected in the myenteric plexus of the intestine. Our study thus shows that i.v. injected adriamycin is distributed preferentially within areas of the PNS where the blood vessels are known to be highly permeable.

Adrenal Medulla↗
PubMed2006

Responding to DNA double strand breaks in the nervous system.

Within the nervous system appropriate responses to DNA damage are required to maintain homeostasis and prevent disease. In this tissue, DNA double-strand breaks (DSBs) initiate a molecular response to repair DNA, or in many cases, activate apoptosis. The repair of DNA DSBs occurs via nonhomologous end-joining (NHEJ) or homologous recombination (HR). These mechanistically distinct pathways are critical for maintenance of genomic integrity. During nervous system development there are discrete requirements for each DNA DSB repair pathway at different stages of development. For example, in the nervous system HR is particularly important for proliferating cells, while NHEJ is critical for differentiating cells. Inactivation of either of these pathways can lead to embryonic lethality, neurodegeneration or brain tumors. Human syndromes that result from defective responses to DNA damage often feature overt neuropathology. A prime example is the neurodegenerative syndrome ataxia telangiectasia (A-T), which results from inactivation of the ATM kinase, a crucial nexus for the cellular response to DNA DSBs. This type of DNA damage activates ATM via the Mre11-Rad50-NBS1 (MRN) complex, which leads to selective phosphorylation of ATM substrates resulting in apoptosis or cell cycle arrest and DNA repair. Furthermore, DNA DSBs resulting from chronic genotoxic stress can also result in tumorigenesis, as inactivation of either HR or NHEJ can lead to certain types of brain tumors. Thus, there are distinct requirements for each DNA DSB repair pathway during neural development, which have important implications for understanding diseases of the nervous system.

Animals↗
PubMed1988

The role of the immune system in central nervous system regeneration (theoretical considerations).

The nervous and immune systems are shown to be interrelated. Steroids inhibit both regeneration and the immune response. Crushing injuries enhance regeneration. A synthesis of these apparently unrelated phenomena is formulated into an immune hypothesis of regeneration. Steroids, in suppressing the immune response, decrease lymphokine production and the subsequent stimulation of nerve cell regeneration. Crushing injuries to nerve fibers cause nerve protein to become antigenic, thereby eliciting the production of "non-toxic" antibodies, which paradoxically protect the nerve fibers from immune attack and cause an augmented lymphokine production and subsequent nerve cell regeneration.

Antibody Formation↗
PubMed2002

[Autonomic nervous system examinations].

Autonomic nervous system plays a critical role in the regulation of cardiovascular system. We reviewed the autonomic nervous system examinations. Time and frequency domain analyses in heart rate variability is obtained from short- and long-term ECG and have predictive values of prognosis in various conditions of heart disease. Baroreflex testing evaluates autonomic modulation of arterial pressure. Baroreflex sensitivity is expressed by the(arterial blood pressure)/(RR interval in ECG) slope in response to infusion of nitroglycerine or phenylephrine. Decrease in baroreflex sensitivity is superior to heart rate variability in identifying patients with poor prognosis in post myocardial infarction. 123I-metaiodobenzylguanidine (MIBG) is an analogue of norepinephrine and hence cardiac 123I-MIBG imaging can visualize cardiac sympathetic nervous system. Defect area in the early phase(15 to 30 min after injection) indicates localization of ventricular denervation. MIBG uptake, measured as a heart to mediastinum activity ratio, had a high predictive vale for survival. Altered MIBG uptake may also play a significant role in the assessment of arrhythmogenic potential in patients with idiopathic ventricular fibrillation or congenital long QT syndrome.

3-Iodobenzylguanidine↗
PubMed1996

Legacy of lead exposure: consequences for the central nervous system.

The central nervous system appears to be the primary target organ for lead. Children in particular remain at risk for the central nervous system effects of lead, not only in many American cities but also in numerous developing countries where the use of leaded gasoline continues. Those same children, moreover, may sustain many of the risk factors, such as low socioeconomic status and calcium and iron insufficiencies, known to exacerbate the manifestations of lead exposure, including its central nervous system effects. Physiologic conditions associated with bone resorption, including pregnancy, lactation, and aging can also potentiate the central nervous system effects of lead and enhance exposure of adults. Questions regarding safe and efficacious diagnosis and treatment of elevated lead burden, particularly as they relate to central nervous system-based effects of lead have recently been raised. Clearly, greater education of and awareness in the medical community are needed for recognition of problems accruing from lead exposure.

Adult↗