THE CEREBROSPINAL FLUID OF LEUKEMIC CHILDREN WITHOUT CENTRAL NERVOUS SYSTEM MANIFESTATIONS

PEDIATRICS ◽  
1963 ◽  
Vol 31 (6) ◽  
pp. 1024-1027
Author(s):  
Audrey E. Evans
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Effective Treatment ◽  
Early Recurrence ◽  
Group I ◽  
The Central Nervous System ◽  
Positive Results

Fifty lumbar punctures were performed on each of three groups of leukemic children. The three categories studied were (1) those with central nervous system manifestations, (2) those free of symptoms following effective treatment, and (3) those not yet having developed central nervous system symptoms. The patients in Group I all had abnormal cerebrospinal fluid. Those examined before or between episodes referable to the central nervous system had normal findings, with rare exceptions. Positive results in the patients without symptoms almost always indicated the early recurrence of central nervous system symptoms.

Effects of acetazolamide on cerebrospinal fluid ions in metabolic alkalosis in dogs

1987 ◽  
Vol 62 (4) ◽  
pp. 1582-1588 ◽  
Author(s):  
S. Javaheri
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Carbonic Anhydrase ◽  
Metabolic Alkalosis ◽  
Renal Effects ◽  
Mechanically Ventilated ◽  
Group I ◽  
The Central Nervous System ◽  
Group Ii

We hypothesized that inhibition of carbonic anhydrase in the central nervous system by acetazolamide should limit the rise in cisternal cerebrospinal fluid (CSF) [HCO3-] observed in metabolic alkalosis. To test this hypothesis, isosmotic isonatremic metabolic alkalosis was produced in two groups of anesthetized, paralyzed, and mechanically ventilated dogs (8 in each group). Group II animals received 50 mg/kg of acetazolamide intravenously 1 h before induction of metabolic alkalosis of 5-h duration. Renal effects of acetazolamide were eliminated by ligation of renal pedicles. In both groups cisternal CSF [Na+] remained relatively constant during metabolic alkalosis. In group I CSF [Cl-] decreased 3.6 and 8.2 meq/l, respectively, 2.5 and 5 h after induction of metabolic alkalosis. Respective increments in CSF [HCO3-] were 3.4 and 6.0 meq/l. In acetazolamide-treated dogs, during metabolic alkalosis, increments in CSF [HCO3-] (4.8 and 7.2 meq/l, respectively, at 2.5 and 5 h) and decrements in CSF [Cl-] (9.1 and 13.3 meq/l) were greater than those observed in group I. We conclude that, in dogs with metabolic alkalosis and bilateral ligation of renal pedicles, acetazolamide impairs CSF regulation of HCO3- and Cl- ions; acetazolamide not only failed to impede HCO3- rise but actually appeared to increase it. The mechanisms for these observations are discussed.

Blumenthal's reaction in cerebrospinal fluid in central nervous system syphilis

1927 ◽  
Vol 23 (8) ◽  
pp. 852-853
Author(s):  
B. I. Serafimov
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
The Central Nervous System ◽  
Positive Results

Having applied this reaction in a number of cases (46) of progressive paralysis, brain syphilis, spinal tapeworm and other diseases of the central nervous system of syphilitic origin, B.I. Serafimov obtained positive results from it in all these cases, - the same as from RW.

Cerebrospinal fluid ions in metabolic acidosis in dogs: effects of acetazolamide

1986 ◽  
Vol 61 (2) ◽  
pp. 633-639 ◽  
Author(s):  
S. Javaheri ◽  
J. Kennealy ◽  
C. D. Runck ◽  
R. G. Loudon ◽  
M. B. Pine ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Mechanical Ventilation ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Metabolic Acidosis ◽  
Control Group ◽  
Acid Base ◽  
Arterial Pco2 ◽  
Group I ◽  
The Central Nervous System

We hypothesized that, during isosmotic isonatremic HCl acidosis with maintained isocapnia in cisternal cerebrospinal fluid (CSF), acetazolamide, by inhibiting carbonic anhydrase (CA) in the central nervous system (CNS), should produce an isonatric hyperchloric metabolic acidosis in CSF. Blood and CSF ions and acid-base variables were measured in two groups of anesthetized and paralyzed dogs with bilateral ligation of renal pedicles during 5 h of HCl acidosis (plasma [HCO3-] = 11 meq/l). Mechanical ventilation was regulated such that arterial PCO2 dropped and CSF Pco2 remained relatively constant. In group I (control group, n = 6), CSF [Na+] remained unchanged, [HCO3-] and strong ions difference (SID) fell, respectively, 6.1 and 5 meq/l, and [Cl-] rose 3.5 meq/l after 5 h of acidosis. In acetazolamide-treated animals, (group II, n = 7), CSF [Na+] remained unchanged, [HCO3-], and SID fell 11 and 7.1 meq/l, respectively, and [Cl-] rose 7.1 meq/l. We conclude that during HCl acidosis inhibition of CNS CA by acetazolamide induces an isonatric hyperchloric metabolic acidosis in CSF, which is more severe than that observed in controls.

Use of a Modified Takata Reaction in the Examination of the Cerebrospinal Fluid of Certain Psychoses

1943 ◽  
Vol 89 (375) ◽  
pp. 297-304 ◽  
Author(s):  
H. H. Fleischhacker
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Liver Disease ◽  
Serum Protein ◽  
The Central Nervous System ◽  
Positive Results ◽  
Degenerative Processes

The Takata reaction has hitherto been mainly applied as a serum protein test and has been claimed useful in the diagnosis of liver disease.It has been modified and applied to the cerebrospinal fluid (Takata-Ara (1)). Preliminary investigators found positive results in syphilis of the central nervous system, and it was thought to be a characteristic of this condition. Subsequent workers, however, found that organic conditions other than neuro-syphilis produced similar positive reactions, with the result that the test fell somewhat into disrepute. Now, however, it seems to be established that the test is indicative of a change in the albumin-globulin (euglobulin) ratios in the cerebrospinal fluid. This condition is mainly found in syphilis of the central nervous system, but occurs, of course, in other conditions affecting the central nervous system, especially where degenerative processes are involved.

CHAPTER 9: Immunology of TBEV-Infections

2020 ◽  
Keyword(s):  
Central Nervous System ◽  
T Cells ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Nk Cells ◽  
Peripheral Blood ◽  
Sample Collection ◽  
Tick Borne Encephalitis ◽  
Viral Infectious Disease ◽  
The Central Nervous System

Tick-borne encephalitis (TBE) is a viral infectious disease of the central nervous system caused by the tick-borne encephalitis virus (TBEV). TBE is usually a biphasic disease and in humans the virus can only be detected during the first (unspecific) phase of the disease. Pathogenesis of TBE is not well understood, but both direct viral effects and immune-mediated tissue damage of the central nervous system may contribute to the natural course of TBE. The effect of TBEV on the innate immune system has mainly been studied in vitro and in mouse models. Characterization of human immune responses to TBEV is primarily conducted in peripheral blood and cerebrospinal fluid, due to the inaccessibility of brain tissue for sample collection. Natural killer (NK) cells and T cells are activated during the second (meningo-encephalitic) phase of TBE. The potential involvement of other cell types has not been examined to date. Immune cells from peripheral blood, in particular neutrophils, T cells, B cells and NK cells, infiltrate into the cerebrospinal fluid of TBE patients.

scholarly journals Development of the Cerebrospinal Fluid in Early Stage after Hemorrhage in the Central Nervous System

Life ◽  
2021 ◽  
Vol 11 (4) ◽  
pp. 300
Author(s):  
Petr Kelbich ◽  
Aleš Hejčl ◽  
Jan Krejsek ◽  
Tomáš Radovnický ◽  
Inka Matuchová ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Early Stage ◽  
Rank Test ◽  
Signed Rank ◽  
Signed Rank Test ◽  
The Central Nervous System ◽  
Poor Outcomes ◽  
Molecular Patterns

Extravasation of blood in the central nervous system (CNS) represents a very strong damaged associated molecular patterns (DAMP) which is followed by rapid inflammation and can participate in worse outcome of patients. We analyzed cerebrospinal fluid (CSF) from 139 patients after the CNS hemorrhage. We compared 109 survivors (Glasgow Outcome Score (GOS) 5-3) and 30 patients with poor outcomes (GOS 2-1). Statistical evaluations were performed using the Wilcoxon signed-rank test and the Mann–Whitney U test. Almost the same numbers of erythrocytes in both subgroups appeared in days 0–3 (p = 0.927) and a significant increase in patients with GOS 2-1 in days 7–10 after the hemorrhage (p = 0.004) revealed persistence of extravascular blood in the CNS as an adverse factor. We assess 43.3% of patients with GOS 2-1 and only 27.5% of patients with GOS 5-3 with low values of the coefficient of energy balance (KEB < 15.0) in days 0–3 after the hemorrhage as a trend to immediate intensive inflammation in the CNS of patients with poor outcomes. We consider significantly higher concentration of total protein of patients with GOS 2-1 in days 0–3 after hemorrhage (p = 0.008) as the evidence of immediate simultaneously manifested intensive inflammation, swelling of the brain and elevation of intracranial pressure.

Chapter 9: Immunology of TBEV-Infection

2021 ◽  
Author(s):  
Sara Gredmark-Russ ◽  
Renata Varnaite
Keyword(s):  
Central Nervous System ◽  
T Cells ◽  
Cerebrospinal Fluid ◽  
Nervous System ◽  
Nk Cells ◽  
Peripheral Blood ◽  
Sample Collection ◽  
Tick Borne Encephalitis ◽  
Viral Infectious Disease ◽  
The Central Nervous System

Tick-borne encephalitis (TBE) is a viral infectious disease of the central nervous system caused by the tick-borne encephalitis virus (TBEV). TBE is usually a biphasic disease and in humans the virus can only be detected during the first (unspecific) phase of the disease. Pathogenesis of TBE is not well understood, but both direct viral effects and immune-mediated tissue damage of the central nervous system may contribute to the natural course of TBE. The effect of TBEV on the innate immune system has mainly been studied in vitro and in mouse models. Characterization of human immune responses to TBEV is primarily conducted in peripheral blood and cerebrospinal fluid, due to the inaccessibility of brain tissue for sample collection. Natural killer (NK) cells and T cells are activated during the second (meningo-encephalitic) phase of TBE. The potential involvement of other cell types has not been examined to date. Immune cells from peripheral blood, in particular neutrophils, T cells, B cells and NK cells, infiltrate into the cerebrospinal fluid of TBE patients.

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