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PubMed2006

Simulation of hemodynamic responses to the valsalva maneuver: an integrative computational model of the cardiovascular system and the autonomic nervous system.

The Valsalva maneuver is a frequently used physiological test in evaluating the cardiovascular autonomic functions in human. Although a large pool of experimental data has provided substantial insights into different aspects of the mechanisms underlying the cardiovascular regulations during the Valsalva maneuver, so far a complete comprehension of these mechanisms and the interactions among them is unavailable. In the present study, a computational model of the cardiovascular system (CVS) and its interaction with the autonomic nervous system (ANS) was developed for the purpose of quantifying the individual roles of the CVS and the ANS in the hemodynamic regulations during the Valsalva maneuver. A detailed computational compartmental parameter model of the global CVS, a system of mathematical equations representing the autonomic nervous reflex regulatory functions, and an empirical cerebral autoregulation (CA) model formed the main body of the present model. Based on simulations of the Valsalva maneuvers at several typical postures, it was demonstrated that hemodynamic responses to the maneuver were not only determined by the ANS-mediated cardiovascular regulations, but also significantly affected by the postural-change-induced hemodynamic alterations preceding the maneuver. Moreover, the large-magnitude overshoot in cerebral perfusion immediately after the Valsalva maneuver was found to result from a combined effect of the circulatory autonomic functions, the CA, and the cerebral venous blood pressure.

Afferent Pathways↗
PubMed2000

Vasculitis of the central nervous system.

Central nervous system (CNS) 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 CNS may be involved in the systemic vasculitides, and neurologic abnormalities occasionally appear as a presenting manifestation of disease. Isolated angiitis of the CNS, a rare form of vasculitis restricted to the CNS, must be distinguished from other causes of CNS inflammation and from noninflammatory vascular disease. We are learning a great deal about the cellular mechanisms of vascular inflammation in the brain. 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 to both pathogenesis of disease and recovery. Two central issues that confront us now are improving the accuracy of the diagnosis (including identifying any underlying infectious causes) and limiting the long-term damage both from disease and its therapies.

Central Nervous System Diseases↗
PubMed2002

[Natural history of the HIV infection and changes in the central nervous system].

Central nervous system (CNS) becomes infected in early days of primary HIV infection. It is concerned to be one of the most important reservoirs of HIV in the human organism. It is also often affected by a number of conditions of different etiology, associated with HIV infection: opportunistic infections, neoplasms, disorders caused by HIV itself, adverse events of drugs, etc. These conditions appear in certain stages of HIV infection, connected with the state of the host's immunological system and degree of immunodeficiency. Unique physiological features of CNS cause that viral replication in CNS is to certain degree independent and different from systemic mechanisms of HIV infection. We overview the natural history of CNS HIV infection and common disorders of CNS associated with HIV regarding the stages of infection and possible mechanisms of viral entry to CNS and its progressive damage.

AIDS-Related Opportunistic Infections↗
PubMedDate not supplied

Electrostimulation of the nervous system for patients with demyelinating and degenerative diseases of the nervous system and vascular diseases of the extremities.

The results of electrostimulation of the spinal cord for symptoms other than that of pain are recorded in this publication. 50% of patients with multiple sclerosis, primary lateral sclerosis and hereditary spino-cerebellar disorders were observed to have enduring favourable changes in neurological function during the 15 to 27 months they have been followed. The patients who were the least severely disabled had the greatest amount of increased function and were benefitted the most by the stimulation. Those who had the fewest neurological pathways affected make the most rapid progress. For example, the patient with only an ataxic or spastic gait was observed to improve faster than the patient with an ataxic and a spastic gait. The long-term effect of electrostimulation of the spinal cord on patients with these diseases is unknown at the present time. The purpose of the stimulation is to increase neurological function so that the patient can live a better life style. It is not thought that the electrical current is responsible for a 'cure' of the basic disease process. Electrostimulation of the posterior spinal roots and spinal cord, while not new, has not been used extensively for the treatment of patients with arterial disease. The patients who have responded the most dramatically to electrostimulation are those with vasospastic disorders. A larger percentage of patients showed a greater response to implanted stimulation than to transcutaneous stimulation. Electrostimulation of the nervous system is not designed to replace standard therapeutic measures of treatment of patients with vascular disease but to supplement them.

Ataxia↗
PubMed2006

[HIV and the central nervous system].

Central nervous system complications are common in HIV-1 infected patients and occur either as a result of concomitant immunosuppression (opportunistic infections, lymphoma and tumors), as a primary manifestation of HIV infection, or as an adverse effect of therapy (immune restoration and toxicity). These complications contribute largely to patient morbidity and mortality. In the era of highly active antiretroviral therapy (HAART) these disease states have changed in presentation, outcome and incidence. We review in detail the epidemiology, pathogenesis, clinical features, diagnosis, and management of these disorders.

AIDS Dementia Complex↗
PubMed2006

The complement system in central nervous system diseases.

The activation of complement system is important factor in inflammatory, neurodegenerative and cerebrovascular diseases. CNS cells are able to synthesize complement components, and myelin and oligodendrocytes (OLG) are known to activate the classical pathway of complement in vitro in the absence of antibodies. Although activation of the complement system is known to promote tissue injury, recent evidence has also indicated that this process can have neuroprotective effects. In particular, terminal C5b-9 complexes enhance OLG survival both in vitro and in vivo. Complement activation may also reduce the accumulation of amyloid and degenerating neurons by promoting their clearance and suggest that certain inflammatory defense mechanisms in the brain may be beneficial in neurodegenerative disease. Complement system activation plays also an important role in brain damage after ischemic injury or head trauma. These findings strongly suggest that complement activation and membrane assembly of C5b-9 can play a role in injury but can also provide neuroprotection depending on the pathophysiological context.

Animals↗
PubMed1998

Vitamin E and other endogenous antioxidants in the central nervous system.

The nervous system is protected from free-radical-induced oxidative damage by a number of antioxidants. These include small-molecular-weight substances such as vitamins C and E as well as the large protein molecules superoxide dismutase, glutathione peroxidase, and others. These antioxidants are often localized in specific portions of the cell. They also show considerable biological interactions with one another. These factors modulate their antioxidant activity. Oxidative stress has been implicated in the pathogenesis of some disorders of the brain; hence, antioxidants have become attractive therapeutic agents. Among the antioxidants, vitamin E has shown some promise in the treatment of Alzheimer's disease and cardiovascular disease. No investigations have been conducted to examine whether vitamin E or other nutritional antioxidants can be used prophylactically to prevent the incidence of degeneration or other pathologic processes in the brain.

Alzheimer Disease↗
PubMed1986

Contribution of vasopressin to vasoconstriction in patients with congestive heart failure: comparison with the renin-angiotensin system and the sympathetic nervous system.

Ten patients with advanced congestive heart failure were treated with an arginine vasopressin V1 antagonist during hemodynamic monitoring to determine the contribution of vasopressin to vasoconstriction in this disorder. The vasopressin antagonist caused a decrease in systemic vascular resistance in the three patients whose plasma vasopressin was greater than 4.0 pg/ml (average for the group was 2.4 +/- 0.6). Plasma vasopressin concentration correlated with the percent decrease of systemic vascular resistance (r = 0.70, p less than 0.025), serum sodium (r = 0.72, p less than 0.02) and serum creatinine (r = 0.85, p less than 0.005). To compare the relative roles of vasopressin, the renin-angiotensin system and the sympathetic nervous system, these patients also received captopril and phentolamine. Captopril decreased systemic vascular resistance by 20% (p less than 0.05), mostly in patients with high plasma renin activity. Levels of plasma renin activity ranged between 1 and 46 ng/ml per h (average 14.7 +/- 5.7) and correlated with serum sodium (r = 0.77, p less than 0.025), serum creatinine (r = 0.73, p less than 0.025) and right atrial pressure (r = 0.67, p less than 0.05). Phentolamine decreased systemic vascular resistance in all patients (average 34%, p less than 0.01), but the decrease did not correlate with the pretreatment norepinephrine concentration. Norepinephrine levels were elevated in all patients (694 +/- 110 pg/ml) and correlated with baseline stroke volume index (r = 0.75, p less than 0.025) and plasma renin activity (r = 0.67, p less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1992

The influence of captopril on the epinephrine response to insulin-induced hypoglycemia in humans. The interaction between the renin-angiotensin system and the sympathetic nervous system.

The aim of this study was to assess whether an interaction exists between the renin-angiotensin system and the sympathetic nervous system at the level of the adrenal medulla during insulin-induced hypoglycemia in normal humans. Seventeen healthy volunteers were studied in a randomized, single-dose, double-blind, cross-over fashion using 25 mg captopril v placebo followed by an intravenous injection of 0.15 IU/kg insulin. Blood samples were obtained before and at 15 min intervals after insulin injection. Both plasma glucose level and heart rate were identical during captopril and placebo at rest and after insulin. Plasma renin activity increased after insulin and captopril. The increase in plasma epinephrine was lower after insulin and captopril compared to after insulin and placebo. Likewise the increase in plasma norepinephrine was blunted on insulin and captopril. Thus, when the generation of angiotensin II was blocked by captopril the insulin-induced rise in epinephrine and norepinephrine was blunted. This indicates that an interaction exists between the renin-angiotensin system and the sympathoadrenal system.

Adult↗
PubMed1994

Effects of lymphoma on the peripheral nervous system.

Peripheral nervous system abnormalities occur in 5% of patients with lymphoma and have a wide differential diagnosis. Herpes zoster is the commonest cause. Vinca alkaloids are the only drugs used in lymphoma which commonly cause neuropathy. Compression or infiltration of nerve roots by lymphoma is a rare presenting feature but becomes more common with advanced disease. Radiation plexopathy does not usually develop until at least 6 months after irradiation and can be difficult to distinguish from neoplastic infiltration. Either multifocal infiltration of nerves or lymphoma-associated vasculitis may present as a peripheral neuropathy. The incidence of Guillain-Barré (GBS) syndrome, and possibly chronic idiopathic demyelinating polyradiculoneuropathy, appears to be increased in association with lymphoma, especially Hodgkin's disease. Subacute sensory neuronopathy and subacute lower motor neuronopathy have both been reported as paraneoplastic syndromes associated with Hodgkin's disease. Treatment of the underlying lymphoma is only rarely followed by recovery of the associated neuropathy.

Antineoplastic Agents↗
PubMed2003

Effects of neuroactive steroids on myelin of peripheral nervous system.

Peripheral nervous system (PNS) possess both classical (e.g. progesterone receptor, PR, androgen receptor, AR) and non-classical (e.g. GABA(A) receptor) steroid receptors and consequently may represent a target for the action of neuroactive steroids. Our data have indicated that neuroactive steroids, like for instance, progesterone, dihydroprogesterone, tetrahydroprogesterone, dihydrotestosterone and 3alpha-diol, stimulate both in vivo and in vitro (Schwann cell cultures), the expression of two important proteins of the myelin of peripheral nerves, the glycoprotein Po (Po) and the peripheral myelin protein 22 (PMP22). It is important to highlight that the mechanisms by which neuroactive steroids exert their effects on the expression of Po and PMP22 involve different kind of receptors depending on the steroid and on the myelin protein considered. In particular, at least in culture of Schwann cells, the expression of Po seems to be under the control of PR, while that of PMP22 needs the GABA(A) receptor. Because Po and PMP22 play an important physiological role for the maintenance of the multilamellar structure of the myelin of the PNS, the present observations might suggest the utilization of neuroactive steroids as new therapeutically approaches for the rebuilding of the peripheral myelin.

Animals↗
PubMed1999

Primary anaplastic large cell lymphoma of the central nervous system.

Central nervous system (CNS) involvement is extremely rare in anaplastic large cell lymphoma (ALCL), and in children only isolated cases have been reported, mainly as secondary CNS involvement. A case of fatal primary ALCL of the brain in a 13-year-old white boy is reported. Magnetic resonance imaging of the brain showed decreased absorption in T1- and T2-weighted image showed a hyperintense signal in the right parietal lobe and 2 masses in the right frontal lobe. A frontal lobe biopsy showed a pleomorphic neoplasm diffusely infiltrating the brain parenchyma and composed of large cells with bizarre, often polylobated or horseshoe-shaped nuclei. Immunohistochemical stains showed diffuse strong positivity for CD30, anaplastic lymphoma kinase protein (ALK-1), p80, leucocyte common antigen, CD45RO (UCHL1), and focal staining for epithelial membrane antigen. Immunostainings for cytokeratins, monocyte-macrophage, and B-cell markers were negative. Epstein-Barr virus latent membrane protein was not detected. To the best of our knowledge, there is only 1 case of primary ALCL of the brain in childhood previously reported in the literature. Before the biopsy, both cases were clinically misdiagnosed as mycobacterial CNS infection. Therefore, primary ALCL should also be included in the differential diagnosis when a mycobacterial CNS infection is suspected in pediatric patients; a careful cytological evaluation of the cerebrospinal fluid or cerebral biopsy are essential for an accurate diagnosis.

Adolescent↗
PubMed1975

Embryonic development and organogenesis in the snail Marisa cornuarietis (Mesogastropoda: Ampullariidae). V. Development of the nervous system.

The nervous system is ectodermal in origin. All nerve ganglia arise separately by proliferation and later delamination from the ectoderm, not by invagination. They become secondarily connected to one another by commissures and connectives developing as extensions from the peripheral layer of ganglionic nerve cells. Rudiments of the cerebral, pedal, pleural and intestinal (parietal) ganglia arise almost simultaneously at a relatively early stage (Stage V). The cerebral ganglia develop from the ectoderm of the head plates. Rudiments of the pedal and pleural ganglia are separate at their inception. They later fuse (Stage VI) to form a pleuro-pedal ganglionic mass on each side. The 2 intestinal ganglia are symmetrical at the beginning, but they soon lose their symmetry as a result of torsion. The right ganglion crosses to the left over the gut and persists as the supraintestinal ganglion. The left or subintestinal ganglion shifts to the right and forward, and fuses with the right pleural ganglion (Stage VIII), thus obscuring the chiastoneury. The paired buccal and single visceral (abdominal) ganglia start differentiating in Stage VII. The former develop from the ectodermal wall of the stomodaeum, while the visceral ganglion delaminates from the right wall of the visceral sac, then shifts to the left during torsion. The statocysts develop early (Stage V) from 2 ectodermal invaginations on either side of the rudimentary foot. They later separate from the overlying ectoderm and statoconi appear in their lumina. Contrary to earlier reports on related ampullariids, the osphradium proved to be ontogenetically older than the mantle and mantle cavity. It starts differentiating as a thickened ectodermal plate in the right wall of the visceral sac (Stage V). During torsion, it becomes engulfed in the mantle cavity and shifts to the left side, then is carried forward as the mantlegrow. The eyes develop late (Stage IX) as ectodermal invaginations which rapidly separate from the ectoderm to form closed vesicles. Their cells start differentiating before hatching to form the retina, in which pigment is deposited, and the inner cornea. The lens is secreted in the lumen of the eye and grows by addition of concentric layers of secretion.

Animals↗
PubMed1992

Structural and functional importance of dietary polyunsaturated fatty acids in the nervous system.

The nervous system is the organ with the second greatest concentration of lipids. These lipids participate directly in membrane functioning. Brain development is genetically programmed. It is therefore necessary to ensure that nerve cells receive an adequate supply of nutrients, especially of lipids, during their differentiation and multiplication, and throughout their lives. The effects of polyunsaturated fatty acid deficiency have been extensively studied; prolonged deficiency leads to death in animals. Linoleic acid is now universally recognized to be an essential nutrient. Until recently, however, alpha-linolenic acid was considered non-essential. Feeding animals with oils that have a low alpha-linolenic content results in all brain cells and organelles and various organs having reduced amounts of 22:6n-3, which is compensated for by an increase in 22:5n-6. The speed of recuperation from these anomalies is extremely slow for brain cells, organelles, and microvessels, in contrast to other organs. A decrease in alpha-linolenic series acids in the membranes results in a 40% reduction in the Na(+)-K(+)-ATPase of nerve terminals and a 20% reduction in 5'-nucleotidase. Some other enzymatic activities are not affected, although membrane fluidity is altered. A diet low in alpha-linolenic acid induces alterations in the electroretinogram which disappear with age; motor function and activity are little affected, but learning behavior is markedly altered. The presence of alpha-linolenic acid in the diet confers a greater resistance to certain neurotoxic agents (triethyl-lead). During the period of cerebral development, there is a linear relationship between brain content of n-3 acids and the n-3 content of the diet up to the point where alpha-linolenic levels reach 200 mg for 100 g of food intake. Beyond that level there is a plateau. For other organs, such as the liver, the relationship is also linear up to 200 mg/100 g, but then there is merely an abrupt change in slope and not a plateau. When dietary 18:2n-6 content was varied, it was noted that 20:4n-6 optimum values were obtained at 150 mg/100 g for all nerve structures, 300 mg for testicle and muscle, 800 mg for kidney, and 1200 mg for liver, lung and heart. A deficiency in alpha-linolenic acid and an excess of linoleic acid have the same main effect: an increase in 22:5n-6 levels.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗