The peripheral nervous system--central nervous system regeneration dichotomy: a role for glial cell transplantation.
Explore the source record for details and available documents.
Animals↗
SEARCH · Search PubMed
Results for “CENTRAL NERVOUS SYSTEM”
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
[AIDS and opportunistic infections of the central nervous system].
Central nervous system diseases occur frequently in patients with AIDS. From 20 to 40% of all these patients develop neurological symptoms and in about 10% of AIDS patients the onset of the disease is characterized by neurological symptoms. These may be related to primary HIV infection or to any of a large number of opportunistic viral and non-viral infections. Moreover, the observation of multiple central nervous system infections is frequent, making the diagnosis difficult. AIDS-related opportunistic infections of the central nervous system are discussed, presenting both a review of the literature and several case reports.
Acquired Immunodeficiency Syndrome↗
[Free radicals in the central nervous system].
Central nervous system has a low antioxidative capacity, which is formed mainly by ascorbic acid. Therefore the cerebral tissue is threatened by the increased formation of free radicals and their metabolites (ROS--reactive oxygen species). ROS are formed such as in reperfusion phase after ischemia and in catecholamine metabolism, in oxidative stress due to hyperglycaemia. Polyunsaturated fatty acids (PUFA) are peroxidased by ROS; proteins and DNK are damaged as well. Free radicals are involved in etiology and pathogenesis of many CNS diseases, such as neuritis, Alzheimer disease, Parkinson disease, Huntington disease, aging and atherosclerosis of the brain, epilepsy, etc. During the antioxidant therapy it is necessary to consider the types of ROS, their origin and their mode of action, whether to administer hydrophilic or lipophilic antioxidants, eventually chelate agents, etc. Hydrophylic antioxidants are acting very soon after the administration, whereas the lipophilic ones reach their target tissues with a great delay. Therefore it is better to apply them preferentially like a prevention, if possible. Enzymatic antioxidants (SOD, GSPHx and catalase and others) are usually acting only for a short time. The methods of estimation of free radicals attacks are discussed as well their possible pathophysiological effects.
Animals↗
Immunolocalization of cathepsin D in the human central nervous system and central nervous system neoplasms.
The cellular distribution of the lysosomal proteinase cathepsin D was studied in a series of 76 neoplasms and 18 non-neoplastic tissues from the human central nervous system, using a well-characterized polyclonal antibody in a peroxidase-antiperoxidase technique. In the normal and developing brain, cathepsin D is confined to neurons and choroid plexus epithelium. Strong granular cytoplasmic staining was present in neuronal and choroid plexus neoplasms, and in reactive macrophages. A large variety of other neoplasms also exhibited positive cytoplasmic staining, albeit usually of a weaker diffuse type. Cathepsin D cannot be considered a specific marker for neuronal or choroid plexus neoplasms, but the antiserum used in this study may be of value in antibody panels for the investigation of these tumours. Its localization may also be of value in embryological studies, particularly in the cerebellum, and in investigations of steroid hormone receptor-associated proteins in meningiomas and Schwannomas.
Brain Neoplasms↗
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↗
[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↗
[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↗
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↗
[Immunology of tumors of the central nervous system].
Central nervous system (CNS) tumours possess special immunological features resulting from their development in an organ having a privileged immunological status. The following review gives a summary of actual data concerning their tumour-associated antigens, the immunological responses of their hosts and the mechanisms permitting them to escape from these responses. There is presently no proof of the existence of tumour-specific antigens on spontaneous glial tumours. Much progress has been made in this area with the development of monoclonal antibodies technology which mainly disclosed the profound antigenic heterogeneity of brain tumours. This heterogeneity could favour the escape of brain tumours from immunosurveillance; furthermore, it represents a major limitation to the use of monoclonal antibodies for diagnosis or therapy. Regarding the immunological responses of brain tumour patients, the main feature is a profound depression of cellular immunity creating an anergic state toward a large number of antigens. In vitro, it concerns specifically T4 helper lymphocytes: their mitogenic responses and secretion of interleukin-2 after antigenic stimuli are drastically reduced. Three phenomena have also been incriminated to explain the defect of immunosurveillance in brain tumour patients: 1) the synthesis by tumour cells of a protective mucopolysaccharidic coat, 2) the secretion by these cells of specific immunosuppressive factors related to cytokines, 3) the isolation of CNS maintained by the blood-brain barrier which regulates the circulation of immunocompetent cells between the intra- and extracerebral compartments. Currents efforts are focused on the individualization of therapy based on these biologic principles.
Antibodies, Monoclonal↗
[Effects of ritodrine hydrochloride on motor nervous system and central nervous system].
Pharmacological effects of ritodrine hydrochloride (ritodrine), a beta 2-adrenoceptor agonist, were investigated in comparison with that of isoxsuprine hydrochloride (isoxsuprine) on the motor nervous system and the central nervous system. Ritodrine (1-30 mg/kg, i.v.) suppressed spontaneous movements in mice, rats and dogs. The animals became slightly sedative and immobile. Ritodrine caused an increase of water intake and vomitting in dogs. These fingings were recovered in 3-5 hr. Isoxsuprine showed similar effects on general behaviour, but the depressive action was more potent than that of ritodrine. Ritodrine slightly suppressed exploratory behaviour in high dose, but had little effect on emotional behaviour. Ritodrine had no effects on conditioned avoidance response, tremor, motor coordination, thiopental induced sleeping time and few types of convulsions. Ritodrine showed no analgetic effects or muscle relaxant actions. Isoxsuprine, in high dose, suppressed motor coordination and showed ataxia. Ritodrine slightly raised body temperature and dose-dependently suppressed hypothermia and ptosis induced by reserpine. Ritodrine (1-10 mg/kg, i.v.) caused a slight resting pattern of spontaneous EEG in rabbits. On the other hand, arousal responses evoked by auditory stimulation, photic stimulation or electrical stimulation of mesencephalic reticular formation were unaffected by ritodrine at any doses used. These results suggest that ritodrine shows little effect on the motor nervous system and central nervous system, and its effects may be nonspecific.
Animals↗
[Non-specific angiitis and the central nervous system].
Central nervous system manifestations of systemic lupus erythematosus are reported in 25 to 60 p. cent of cases and include mental disturbances, epilepsy, focal deficits, and headache. Cerebrospinal fluid (CSF) changes are inconstantly observed. Cerebral scintigraphy may be useful. CT Scan imaging shows infarcts, hemorrhages, or cortical atrophy. Cerebral angiography is usually normal. Pathological examination shows frequent arteriolar lesions in the CNS but their appearance is rarely that of an angiitis. The mechanism of the CNS lesion involves both angiitis and antineuronal antibodies. Diagnosis is difficult when presenting signs are those of CNS involvement, particularly as the ESR can be normal. Serum complement and anti-DNA antibody levels are frequently normal when there is an isolated CNS involvement. Overall prognosis is poor in cases with CNS lesions. The use of corticoids is discussed. Cerebral angiitis is an exceptional finding during the course of rheumatoid arthritis and scleroderma. Central neurological manifestations of Sharp's and Gougerot-Sjögren's syndromes have recently been reported. CNS lesions are reported in 10 to 20 p. cent of patients with panarteritis nodosa and include mental disorders and disturbance of vigilance, epilepsy, focal deficits, meningeal signs and headache. The CSF is often normal. The CT scan provides images of infarcts, hemorrhages or cortical atrophy. Cerebral angiography may show segmental stenoses and distal occlusions. Pathological examination of the CNS shows mainly lesions in the intracerebral and leptomeningeal arterioles and small caliber arteries. Treatment is by corticoids and immunosuppressors. Angiitis of the CNS is rare and of late onset in Wegener's granulomatosis. Hypersensitivity angiitis rarely affects the CNS, those cases where it is involved being of poor prognosis and probably related to panarteritis nodosa. CNS manifestations in giant cell arteritis and Takayasu's arteritis result from neck artery lesions. The CNS is affected in 20 p. cent of cases in Behcet's disease with resulting isolated aseptic meningitis or a meningo-encephalomyelitis, and intracranial hypertension. The CSF is nearly always abnormal. Cerebral angiography should be directed towards the search for cerebral thrombophlebitis. Pathologically lesions predominate in the brain stem. Meningeal lesions are almost constantly present. Neurological involvement is of poor prognosis, and early corticotherapy must be instituted. The nosological autonomy of Buerger's thromboangiitis obliterans is questioned. Lymphomatoid granulomatosis is a particular type of angiitis in which malignant cell infiltration occurs. The CNS is affected in 20 p. cent of cases, and whatever the treatment the prognosis is poor. Granulomatous angiitis of the CNS has the distinctive feature of lesions affecting the CNS vessels either exclusively or predominantly. The antemortem diagnosis is based on biopsy of the leptomeninges, and treatment with corticoids and immunosuppressors may prove effective.
Cerebrovascular Disorders↗
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↗
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↗
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↗
[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↗
Aromatase in the central nervous system.
Central (central nervous system and pituitary) aromatization appears to be a fundamental process for endocrine control and development. Metabolism of androgens to estrogens and the subsequent metabolism of estrogens have been proven in many species, including humans, and linked to estrogen action. Thus, aromatization appears to initiate or to be involved in activities of importance to endocrine function at the central level and their effects peripherally. In the context of breast cancer, central aromatization relates to the control of gonadotrophins and other pituitary-brain hormones which may effect metabolism at the level of the breast. For example, follicle-stimulating hormone can increase aromatization and may be a factor in the control of such metabolism in breast tissue.
Androgens↗