Cerebrospinal Fluid Alterations Associated with Central Nervous System Infections

Labadie, Enrique L.

doi:10.1007/978-1-4684-1039-6_31

Cited by 5 publications

(4 citation statements)

References 170 publications

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“…Glucose enters the CSF by a facilitated transport system located in the choroid plexus (6)(7)(8)(9). It has been shown that CSF glucose levels are directly related to concentrations of glucose in the blood (1,10). The correlation between the blood and CSF glucose concentrations was also seen in our study.…”

Section: Discussionsupporting

confidence: 80%

“…Hyperglycaemia associated with FCs has been reported to be of short duration, since 2 h after the seizure the blood glucose levels had already returned to normal (2). The facts that the elevation in the CSF glucose level follows the change in blood glucose (10) and that the decrease in glucose concentrations is more rapid in blood than in the CSF (10, 1 l), can at least partly explain our observation that the changes in glucose levels are more evident in the CSF than in blood. A higher CSF glucose concentration during fever cannot be explained by dehydration and the concentration of the CSF, since the osmolality in the CSF was lowest when it was associated with the highest glucose concentrations.…”

Section: Discussionmentioning

confidence: 49%

“…The correlation between the blood and CSF glucose concentrations was also seen in our study. Acute elevations in blood glucose levels are reflected in the CSF within 60-120 min (10). Hyperglycaemia associated with FCs has been reported to be of short duration, since 2 h after the seizure the blood glucose levels had already returned to normal (2).…”

Section: Discussionmentioning

confidence: 99%

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The role of fever on cerebrospinal fluid glucose concentration of children with and without convulsions

Kiviranta

Tuomisto

1995

Acta Paediatrica

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FinlundKiVirdnta T, Airaksinen EM, Tuomisto L. The role of fever on cerebrospinal fluid glucose concentration of children with and without convulsions. Acta Prediatr 1995;84: 1276-9. Stockholm.In febrile convulsions glucose concentrations are known to increase both in the blood and cerebrospinal fluid (CSF). The reason behind this increase is, however, incompletely understood. We have studied the effects of convulsion and fever on the CSF and blood glucose concentrations in four different groups of children: febrile and non-febrile children, with and without convulsions. The concentration of glucose in the CSF was significantly higher in febrile children with (4.4 f 0.1 mmol/l, mean f SEM n = 35, p < 0.01, ANOVA, Duncan's test) and without convulsions (3.9 f 0.2mmol/l, n = 22, p < 0.05) than in non-febrile, non-convulsive children (3.3 k 0.1 mmol/l, n = 21). In nonfebrile convulsive children, the CSF glucose concentration was 3.7 f 0.2mmol/l (n = 10). Both fever and seizures increased the CSF glucose levels (p < 0.0001 and p = 0.028, respectively, analysis of covariance). There was a linear correlation between the body temperature and concentration of glucose in the CSF ( r = 0.454, p < 0.0001, n = 88, Pearson's correlation analysis). The changes in blood glucose concentrations between the groups parallelled those found in the CSF. Our results show that hyperglycdemia and an increase in the CSF glucose concentration in febrile convulsions is not explained just by a stress reaction, evoked by the seizure, as has been hypothesized earlier, but by the influence of increased body temperature as well. 0 Cerehrospinal~uid,,f~hrile convulsion,,fevrr, glucose, seizure T Kivirunta,

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 49%

Section: Discussionmentioning

confidence: 99%

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The role of fever on cerebrospinal fluid glucose concentration of children with and without convulsions

Kiviranta

Tuomisto

1995

Acta Paediatrica

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“…However, the postpartum onset of binge eating and violent behavior suggests a change in her CNS function at that time. Hypoglycorrhachia in adults is usually secondary to one of a large variety of CNS infections (Labadie, 1980), although no history of such an infection was obtained in this patient. Inherited or congenital glucose transport defects would likely have been associated with earlier neurological problems (DeVivo et al, 1991).…”

Section: Disc Ussl Onmentioning

confidence: 99%

Fasting and postprandial cerebrospinal fluid glucose concentrations in healthy women and in an obese binge eater

Geracioti

Loosen

Ebert

et al. 1995

Int. J. Eat. Disord.

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Objective: We hypothesized that abnormal entry of glucose into the central nervous system (CNS) might exist in some chronic binge eaters of carbohydrates, as either a cause or consequence of binge eating. The purpose of this study was thus to determine fasting and postprandial glucose concentrations in the cerebrospinal fluid (CSF) of healthy women, and to obtain similar data in an obese, irritable woman with chronic binge eating of postpartum onset. Method: CSF was sampled continuously at 0.1 ml/min from 1100 hr to 1700 hr from the binge eating patient, who consumed 5,000 to 10,000 calories per day (preferentially binging on refined carbohydrates), and 4 healthy women via an indwelling, flexible spinal canal catheter. CSF aliquots were obtained at 10‐min intervals for measurement of glucose concentrations. Simultaneously, blood was withdrawn at 30‐min intervals to obtain serum for glucose assay. A glucose‐rich mixed liquid meal was consumed by participants at 1300 hr. Results: In striking contrast to the normal women, our bulimic patient showed no postprandial rise whatever in CSF glucose concentrations. Fasting CSF glucose concentrations were slightly lower whereas fasting serum glucose levels were normal in the bulimic patient, compared with the normal women. After eating, serum glucose levels increased in all participants, but less so in our patient. Discussion: This is the first description of a lack of postprandial elevation in CSF glucose concentration in a patient with a binge eating disorder. Defective transport of glucose across the blood‐brain barrier might account for the observed abnormality. While considering other possiblities, we conjecture that our patient's binge eating was an attempt to compensate for impaired postprandial entry of glucose into her CNS. © 1995 by John Wiley & Sons, Inc.

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Cerebrospinal Fluid Alterations Associated with Central Nervous System Infections

Cited by 5 publications

References 170 publications

The role of fever on cerebrospinal fluid glucose concentration of children with and without convulsions

The role of fever on cerebrospinal fluid glucose concentration of children with and without convulsions

Fasting and postprandial cerebrospinal fluid glucose concentrations in healthy women and in an obese binge eater

Survival Improvement in Coccidioidal Meningitis by High-Dose Intrathecal Amphotericin B

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