Abnormalities of cerebrospinal fluid amino-acids in purulent meningitis

Corston, R N; McGale, E.H.F.; Stonier, C.; Hutchinson, Edward; Aber, G. M.

doi:10.1136/jnnp.42.10.881

Cited by 17 publications

(8 citation statements)

References 19 publications

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“…No significant changes were noted in the amino-acid concentrations in sheep CSF, either with disease or age (Table 3) and these were within the range of control values reported in humans (Corston et al, 1979; Gårseth et al, 2001; Peng et al, 2005; Rothrock et al, 1995). This contrasts with changes in CSF amino acid concentrations noted in other diseases including increased glutamate concentrations in ALS (Spreux-Varoquaux et al, 2002) and HIV dementia (Ferrarese et al, 2001), and significant changes in neuroactive compounds such as glutamate, taurine and glycine in patients with polyradiculoneuropathy (Gårseth et al, 2001).…”

Section: Discussionsupporting

confidence: 76%

Neuropeptide changes and neuroactive amino acids in CSF from humans and sheep with neuronal ceroid lipofuscinoses (NCLs, Batten disease)

Kay

Verbeek

Furlong

et al. 2009

Neurochemistry International

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Anomalies in neuropeptides and neuroactive amino acids have been postulated to play a role in neurodegeneration in a variety of diseases including the inherited neuronal ceroid lipofuscinoses (NCLs, Batten disease). These are often indicated by concentration changes in cerebrospinal fluid (CSF). Here we compare CSF neuropeptide concentrations in patients with the classical juvenile CLN3 form of NCL and the classical late infantile CLN2 form with neuropeptide and neuroactive amino acid concentrations in CSF from in sheep with the late infantile variant CLN6 form. A marked disease related increase in CSF concentrations of neuron specific enolase and tau protein was noted in the juvenile CLN3 patients but this was not observed in an advanced CLN2 patient nor CLN6 affected sheep. No changes were noted in S-100b, GFAP or MBP in patients or of S-100b, GFAP or IGF-1 in affected sheep. There were no disease related changes in CSF concentrations of the neuroactive amino acids, aspartate, glutamate, serine, glutamine, glycine, taurine and GABA in these sheep. The changes observed in the CLN3 patients may be progressive markers of neurodegeneration, or of underlying metabolic changes perhaps associated with CLN3 specific changes in neuroactive amino acids, as have been postulated. The lack of changes in the CLN2 and CLN6 subjects indicate that these changes are not shared by the CLN2 or CLN6 forms and changes in CSF concentrations of these compounds are unreliable as biomarkers of neurodegeneration in the NCLs in general.

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Section: Discussionsupporting

confidence: 76%

Neuropeptide changes and neuroactive amino acids in CSF from humans and sheep with neuronal ceroid lipofuscinoses (NCLs, Batten disease)

Kay

Verbeek

Furlong

et al. 2009

Neurochemistry International

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“…These findings extend previous studies that have documented increased CSF concentrations of glutamate, aspartate, glycine, taurine, and alanine in patients with bacterial meningitis (18,20). Increased concentrations of other individual amino acids, as well as of the total concentration of amino acids, have also been observed in patients with meningitis (17,19,28). One study documented that patients with high CSF concentrations of amino acids had an increased incidence of death or neurologic sequelae, but no correlation was found in that study between amino acid concentrations and CSF leukocyte, lactate, or protein concentrations in the relatively small number of patients studied (28).…”

Section: Discussionmentioning

confidence: 94%

“…This may, however, not be the only factor for at least two reasons. Concentrations of amino acids can be higher in the CSF than in serum during meningitis, indicating an additional intracranial source, and previous studies have not found a good correlation between CSF amino acid concentrations and CSF protein concentrations, which represent a good marker for blood-brain barrier disruption (19,28,30). Increases in CSF protein concentrations have been well documented in our model of meningitis, but we have not measured CSF protein concentrations in the present study.…”

Section: Discussionmentioning

confidence: 99%

“…A first report in 1975 found increased levels of glutamic acid, glutamine, and y-aminobutyric acid in the CSF of patients with bacterial meningitis (1 7). Other authors have also reported abnormal CSF concentrations of amino acids, but the importance of these changes has not been explored in detail (18)(19)(20). Importantly, it is not known whether amino acid concentrations in the CSF reflect changes occurring in the brain interstitial fluid, the medium relevant for the potential neurotoxicity of EAA.…”

Section: The Infectious Diseases Laboratories [Lg-r Jh T Mamentioning

confidence: 99%

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Amino Acids in Cerebrospinal and Brain Interstitial Fluid in Experimental Pneumococcal Meningitis

et al. 1993

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ABSTRACT. Excitatory amino acids are increasingly implicated in the pathogenesis of neuronal injury induced by a variety of CNS insults, such as ischemia, trauma, hypoglycemia, and epilepsy. Little is known about the role of amino acids in causing CNS injury in bacterial meningitis. Several amino acids were measured in cerebrospinal fluid and in microdialysis samples from the interstitial fluid of the frontal cortex in a rabbit model of pneumoccocal meningitis. Cerbrospinal fluid concentrations of glutamate, aspartate, glycine, taurine, and alanine increased significantly in infected animals. Among the amino acids with known excitatory or inhibitory function, interstitial fluid concentrations of glutamate were significantly elevated (by 470%).Alanine, a marker for anaerobic glycolysis, also increased in the cortex of infected rabbits. The elevated glutamate concentrations in the brain extracellular space suggest that excitotoxic neuronal injury may play a role in bacterial meningitis. (Pediatr Res 33: 510-513, 1993) Abbreviations CSF, cerebrospinal fluid EAA, excitatory amino acid cfu, colony-forming unit poorly understood. Cerebral blood flow studies in humans and experimental animals with bacterial meningitis suggest that, after an initial hyperemic phase (13), ischemia occurs under certain circumstances and may contribute to the development of neuronal injury (14-16). As with other forms of ischemia-induced CNS injury it is conceivable that the harmful effects of ischemia could be potentiated by EAA during meningitis.A few studies have examined concentrations of amino acids in CSF in bacterial meningitis. A first report in 1975 found increased levels of glutamic acid, glutamine, and y-aminobutyric acid in the CSF of patients with bacterial meningitis (1 7). Other authors have also reported abnormal CSF concentrations of amino acids, but the importance of these changes has not been explored in detail (18)(19)(20). Importantly, it is not known whether amino acid concentrations in the CSF reflect changes occurring in the brain interstitial fluid, the medium relevant for the potential neurotoxicity of EAA. To test the hypothesis that changes in amino acids may play a role in CNS injury during meningitis, we measured in the present study brain interstitial fluid concentrations of several amino acids in a rabbit model of pneumoccoca1 meningitis and determined whether changes similar to those observed in the CSF during meningitis occur in the brain. Interstitial fluid concentrations of amino acids were measured in the cortex because of its proximity to the inflammation in the subarachnoid space and because pathologic changes were primarily found in the cortex in a recent histopathologic study in rats with experimental pneumococcal meningitis (2 1).EAA, physiologic neurotransmitters in the mammalian CNS, are increasingly implicated in the pathogenesis of neuronal injury induced by a variety of CNS insults, such as global and focal ischemia, brain and spinal cord trauma, hypoglycemia, and epilepsy (1-7). There is good...

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“…Period I contains all values from the first day of clinical symptoms to day 7 of illness (mean 5 Table 2. Full data can be obtained from the authors (RNC).…”

Section: Methodsmentioning

confidence: 99%

Cerebrospinal fluid amino acid concentrations in patients with viral and tuberculous meningitis.

Corston¹,

McGale²,

Stonier³

et al. 1981

Journal of Neurology, Neurosurgery & Psychiatry

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Abnormalities of cerebrospinal fluid amino-acids in purulent meningitis

Cited by 17 publications

References 19 publications

Neuropeptide changes and neuroactive amino acids in CSF from humans and sheep with neuronal ceroid lipofuscinoses (NCLs, Batten disease)

Neuropeptide changes and neuroactive amino acids in CSF from humans and sheep with neuronal ceroid lipofuscinoses (NCLs, Batten disease)

Amino Acids in Cerebrospinal and Brain Interstitial Fluid in Experimental Pneumococcal Meningitis

Cerebrospinal fluid amino acid concentrations in patients with viral and tuberculous meningitis.

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