Neuroactive kynurenines in lyme borreliasis

John Halperin, Melvyn P. Heyes

Research output: Contribution to journalArticle

95 Citations (Scopus)

Abstract

Although neurologic dysfunction occurs frequently in patients with Lyme borreliosis it is rarely possible to demonstrate the causative organism within the neuraxis. Thisdiscordance could arise if neurologic symptoms were actually due to soluble neuromodulators produced in response to infection. Since immune stimulation is associated with the production of quinolinic acid (QUIN) an excitotoxin and N-methyl-D-aspartate (NMDA) agonist we measured levels of CSF and serum QUIN and lymphokines. Samples were obtained from 16 patients with CNS Borrelia burgdorferi infection, eight patients with Lyme encephalopathy (confusion without intra-CNS inflammation) and 45 controls. CSF QUIN was substantially elevated in patients with CNS Lyme and correlated strongly with CSF leukocytosis. In patients with encephalopathy, serum QUIN was elevated with corresponding increments in CSF QUIN. Lymphokine concentrations were not consistently elevated. We conclude that CSF QUIN is significantly elevated in B burgdorferi infection—dramatically in patients with CNS inflammation less in encephalopathy. The presence of this known agonist of NMDA synaptic function—a receptor involved in learning, memoryand synaptic plasticity—may contribute to the neurologic and cognitive deficits seen in many Lyme disease patients.

Original languageEnglish (US)
Pages (from-to)43-50
Number of pages8
JournalNeurology
Volume42
Issue number1
StatePublished - Jan 1 1992
Externally publishedYes

Fingerprint

Kynurenine
Quinolinic Acid
Brain Diseases
Neurologic Manifestations
Lyme Disease
Lymphokines
N-Methylaspartate
Borrelia Infections
Inflammation
Confusion
Neurotransmitter Receptor
Borrelia burgdorferi
Leukocytosis
Neurotoxins
Serum
Neurotransmitter Agents
Learning
Infection

All Science Journal Classification (ASJC) codes

  • Clinical Neurology

Cite this

Halperin, J., & Heyes, M. P. (1992). Neuroactive kynurenines in lyme borreliasis. Neurology, 42(1), 43-50.
Halperin, John ; Heyes, Melvyn P. / Neuroactive kynurenines in lyme borreliasis. In: Neurology. 1992 ; Vol. 42, No. 1. pp. 43-50.
@article{82f84d3060564b7886e0eedba072e6de,
title = "Neuroactive kynurenines in lyme borreliasis",
abstract = "Although neurologic dysfunction occurs frequently in patients with Lyme borreliosis it is rarely possible to demonstrate the causative organism within the neuraxis. Thisdiscordance could arise if neurologic symptoms were actually due to soluble neuromodulators produced in response to infection. Since immune stimulation is associated with the production of quinolinic acid (QUIN) an excitotoxin and N-methyl-D-aspartate (NMDA) agonist we measured levels of CSF and serum QUIN and lymphokines. Samples were obtained from 16 patients with CNS Borrelia burgdorferi infection, eight patients with Lyme encephalopathy (confusion without intra-CNS inflammation) and 45 controls. CSF QUIN was substantially elevated in patients with CNS Lyme and correlated strongly with CSF leukocytosis. In patients with encephalopathy, serum QUIN was elevated with corresponding increments in CSF QUIN. Lymphokine concentrations were not consistently elevated. We conclude that CSF QUIN is significantly elevated in B burgdorferi infection—dramatically in patients with CNS inflammation less in encephalopathy. The presence of this known agonist of NMDA synaptic function—a receptor involved in learning, memoryand synaptic plasticity—may contribute to the neurologic and cognitive deficits seen in many Lyme disease patients.",
author = "John Halperin and Heyes, {Melvyn P.}",
year = "1992",
month = "1",
day = "1",
language = "English (US)",
volume = "42",
pages = "43--50",
journal = "Neurology",
issn = "0028-3878",
publisher = "Lippincott Williams and Wilkins",
number = "1",

}

Halperin, J & Heyes, MP 1992, 'Neuroactive kynurenines in lyme borreliasis', Neurology, vol. 42, no. 1, pp. 43-50.

Neuroactive kynurenines in lyme borreliasis. / Halperin, John; Heyes, Melvyn P.

In: Neurology, Vol. 42, No. 1, 01.01.1992, p. 43-50.

Research output: Contribution to journalArticle

TY - JOUR

T1 - Neuroactive kynurenines in lyme borreliasis

AU - Halperin, John

AU - Heyes, Melvyn P.

PY - 1992/1/1

Y1 - 1992/1/1

N2 - Although neurologic dysfunction occurs frequently in patients with Lyme borreliosis it is rarely possible to demonstrate the causative organism within the neuraxis. Thisdiscordance could arise if neurologic symptoms were actually due to soluble neuromodulators produced in response to infection. Since immune stimulation is associated with the production of quinolinic acid (QUIN) an excitotoxin and N-methyl-D-aspartate (NMDA) agonist we measured levels of CSF and serum QUIN and lymphokines. Samples were obtained from 16 patients with CNS Borrelia burgdorferi infection, eight patients with Lyme encephalopathy (confusion without intra-CNS inflammation) and 45 controls. CSF QUIN was substantially elevated in patients with CNS Lyme and correlated strongly with CSF leukocytosis. In patients with encephalopathy, serum QUIN was elevated with corresponding increments in CSF QUIN. Lymphokine concentrations were not consistently elevated. We conclude that CSF QUIN is significantly elevated in B burgdorferi infection—dramatically in patients with CNS inflammation less in encephalopathy. The presence of this known agonist of NMDA synaptic function—a receptor involved in learning, memoryand synaptic plasticity—may contribute to the neurologic and cognitive deficits seen in many Lyme disease patients.

AB - Although neurologic dysfunction occurs frequently in patients with Lyme borreliosis it is rarely possible to demonstrate the causative organism within the neuraxis. Thisdiscordance could arise if neurologic symptoms were actually due to soluble neuromodulators produced in response to infection. Since immune stimulation is associated with the production of quinolinic acid (QUIN) an excitotoxin and N-methyl-D-aspartate (NMDA) agonist we measured levels of CSF and serum QUIN and lymphokines. Samples were obtained from 16 patients with CNS Borrelia burgdorferi infection, eight patients with Lyme encephalopathy (confusion without intra-CNS inflammation) and 45 controls. CSF QUIN was substantially elevated in patients with CNS Lyme and correlated strongly with CSF leukocytosis. In patients with encephalopathy, serum QUIN was elevated with corresponding increments in CSF QUIN. Lymphokine concentrations were not consistently elevated. We conclude that CSF QUIN is significantly elevated in B burgdorferi infection—dramatically in patients with CNS inflammation less in encephalopathy. The presence of this known agonist of NMDA synaptic function—a receptor involved in learning, memoryand synaptic plasticity—may contribute to the neurologic and cognitive deficits seen in many Lyme disease patients.

UR - http://www.scopus.com/inward/record.url?scp=0026542519&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0026542519&partnerID=8YFLogxK

M3 - Article

C2 - 1531156

AN - SCOPUS:0026542519

VL - 42

SP - 43

EP - 50

JO - Neurology

JF - Neurology

SN - 0028-3878

IS - 1

ER -