Cerebrospinal Fluid Enzymes in Neurological Disease

1983 ◽  
pp. 205-231 ◽  
Author(s):  
Naren L. Banik ◽  
Edward L. Hogan
Keyword(s):  
Cerebrospinal Fluid ◽  
Neurological Disease

scholarly journals Cerebrospinal fluid extracellular vesicle enrichment for protein biomarker discovery in neurological disease; multiple sclerosis

2017 ◽  
Vol 6 (1) ◽  
pp. 1369805 ◽  
Author(s):  
Joanne L. Welton ◽  
Samantha Loveless ◽  
Timothy Stone ◽  
Chris von Ruhland ◽  
Neil P. Robertson ◽  
...  
Keyword(s):  
Multiple Sclerosis ◽  
Cerebrospinal Fluid ◽  
Neurological Disease ◽  
Biomarker Discovery ◽  
Extracellular Vesicle ◽  
Protein Biomarker

Identification of Sarcocystis capracanis in cerebrospinal fluid from sheep with neurological disease

2013 ◽  
Vol 193 (1-3) ◽  
pp. 252-255 ◽  
Author(s):  
P. Formisano ◽  
B. Aldridge ◽  
Y. Alony ◽  
L. Beekhuis ◽  
E. Davies ◽  
...  
Keyword(s):  
Cerebrospinal Fluid ◽  
Neurological Disease

External Ventricular Drainage

2018 ◽  
pp. 165-172
Author(s):  
Nitin Agarwal ◽  
Andrew F. Ducruet
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebrospinal Fluid ◽  
Neurological Disease ◽  
External Ventricular Drain ◽  
Management Strategies ◽  
External Ventricular Drainage ◽  
Postoperative Management ◽  
Ventricular Drainage ◽  
Cerebrospinal Fluid Diversion ◽  
Lumbar Drain

External ventricular drainage, or ventriculostomy, refers to surgical placement of a catheter into the ventricle to achieve temporary cerebrospinal fluid diversion and remains one of the most frequently performed neurosurgical interventions. External ventricular drainage is an essential therapeutic strategy for a myriad of neurological disease processes causing hydrocephalus or increased intracranial pressure including traumatic brain injury, subarachnoid hemorrhage, and intracranial hemorrhage with intraventricular extension. In select cases, lumbar drains may provide a suitable alterative to an external ventricular drain (EVD). Complications related to both EVD and lumbar drain placement include malfunction, infection, and hemorrhage. This chapter reviews the indications, surgical technique, postoperative management strategies, and potential complications associated with external ventricular drainage.

Upper reference limits for cerebrospinal fluid total protein and albumin quotient based on a large cohort of control patients: implications for increased clinical specificity

2016 ◽  
Vol 54 (2) ◽  
Author(s):  
Harald Hegen ◽  
Michael Auer ◽  
Achim Zeileis ◽  
Florian Deisenhammer
Keyword(s):  
Cerebrospinal Fluid ◽  
Total Protein ◽  
Neurological Disease ◽  
Large Cohort ◽  
Barrier Dysfunction ◽  
Serum Samples ◽  
Age Related ◽  
Reference Limits ◽  
Future Revision ◽  
Work Up

AbstractDetermination of cerebrospinal fluid (CSF) total protein (TP) as well as of CSF/serum albumin quotient (Qalb) is part of the routine CSF work-up. However, currently used upper reference limits (URL) are not well validated leading to over-reporting of blood-CSF barrier dysfunction in approximately 15% of patients without neurological disease. The objective of this study was to determine age-related URL for CSF TP and Qalb in a cohort of control patients.A total of 332 paired CSF and serum samples of patients without objective clinical and paraclinical findings of a neurological disease were analyzed for CSF TP and Qalb. CSF TP was measured by spectrophotometry and albumin in CSF and serum by nephelometry.CSF TP concentration and Qalb significantly correlated with age. In subjects at the age of 18–70 years, median CSF TP ranged from 320 to 460 mg/L and URL defined as the 95th percentile were 530–690 mg/L. Median Qalb ranged from 4.1 to 6.1 and URL from 8.7 up to 11.0. For URL of Qalb we calculated the following formula: age/25+8.Age-dependent URL for CSF TP and Qalb are presented here in a large cohort of control patients. They are higher than those currently recommended and this probably explains why isolated blood-CSF barrier dysfunction has been apparently over-reported. These new URL might be considered in a future revision of CSF guidelines.

scholarly journals Compartmentalization and Clonal Amplification of HIV-1 Variants in the Cerebrospinal Fluid during Primary Infection

2009 ◽  
Vol 84 (5) ◽  
pp. 2395-2407 ◽  
Author(s):  
Gretja Schnell ◽  
Richard W. Price ◽  
Ronald Swanstrom ◽  
Serena Spudich
Keyword(s):  
Cerebrospinal Fluid ◽  
Neurological Disease ◽  
Primary Infection ◽  
Genetic Adaptation ◽  
Variable Regions ◽  
Single Genome ◽  
Immunodeficiency Virus ◽  
The Central Nervous System ◽  
Hiv 1

ABSTRACT Human immunodeficiency virus type 1 (HIV-1)-associated dementia (HAD) is a severe neurological disease that affects a subset of HIV-1-infected individuals. Increased compartmentalization has been reported between blood and cerebrospinal fluid (CSF) HIV-1 populations in subjects with HAD, but it is still not known when compartmentalization arises during the course of infection. To assess HIV-1 genetic compartmentalization early during infection, we compared HIV-1 populations in the peripheral blood and CSF in 11 primary infection subjects, with analysis of longitudinal samples over the first 18 months for a subset of subjects. We used heteroduplex tracking assays targeting the variable regions of env and single-genome amplification and sequence analysis of the full-length env gene to identify CSF-compartmentalized variants and to examine viral genotypes within the compartmentalized populations. For most subjects, HIV-1 populations were equilibrated between the blood and CSF compartments. However, compartmentalized HIV-1 populations were detected in the CSF of three primary infection subjects, and longitudinal analysis of one subject revealed that compartmentalization during primary HIV-1 infection was resolved. Clonal amplification of specific HIV-1 variants was identified in the CSF population of one primary infection subject. Our data show that compartmentalization can occur in the central nervous system (CNS) of subjects in primary HIV-1 infection in part through persistence of the putative transmitted parental variant or via viral genetic adaptation to the CNS environment. The presence of distinct HIV-1 populations in the CSF indicates that independent HIV-1 replication can occur in the CNS, even early after HIV-1 transmission.

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