Neurochemical Alterations in Cerebrospinal Fluid in Cerebral Ischemia and Stroke

Welch, K. M. A.; Meyer, John Stirling

doi:10.1007/978-1-4684-1039-6_24

Cited by 8 publications

(5 citation statements)

References 41 publications

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“…The pattern of increase of amino acid concentrations was similar to that in microdialysates of the extracellular fluid in cerebral cortex and striatum after hypoxic-ischemia in fetal lambs (9), newborn rats (10) or adult animals (30,31). However, the concentration of amino acids in lumbar CSF may not directly reflect events in the brain (33)(34)(35). Asphyxia-induced alterations in the spinal cord or a leaky blood-brain barrier could modify amino acid concentrations measured in the CSF (34,36).…”

Section: Discussionmentioning

confidence: 75%

“…However, the concentration of amino acids in lumbar CSF may not directly reflect events in the brain (33)(34)(35). Asphyxia-induced alterations in the spinal cord or a leaky blood-brain barrier could modify amino acid concentrations measured in the CSF (34,36). Red blood cells, and to some extent proteins, were higher in the CSF of asphyxiated infants but did not differ significantly from the levels in the control group.…”

Section: Discussionmentioning

confidence: 99%

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Excitatory amino acids in the cerebrospinal fluid of asphyxiated infants: relationship to hypoxic‐ischemic encephalopathy

et al. 1993

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Asphyxiated (n = 27) and control infants (n = 25) were subjected to spinal taps. Amino acids were measured with liquid chromatography and the degree of hypoxic-ischemic encephalopathy was determined in each case. In asphyxiated infants, the concentrations of aspartate and glutamate were 286% and 387% (p < or = 0.01 and p < or = 0.05) of the control values, respectively. The cerebrospinal fluid aspartate levels were significantly (p < or = 0.05) higher in the group with severe (3.4 mumol/l) compared with the group with mild hypoxic-ischemic encephalopathy (1.0 mumol/l). Glutamate was also higher in the group with severe (12.3 mumol/l) than in the groups with mild (2.7 mumol/l) or moderate (3.2 mumol/l) hypoxic-ischemic encephalopathy (p < or = 0.05). High concentrations of excitatory amino acids were present in the CSF of asphyxiated infants which may exert excitotoxic effects.

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Section: Discussionmentioning

confidence: 75%

Section: Discussionmentioning

confidence: 99%

Excitatory amino acids in the cerebrospinal fluid of asphyxiated infants: relationship to hypoxic‐ischemic encephalopathy

et al. 1993

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“…There may be more than one reason for altered concentrations of monoamine metabolites in CSF after cerebral ischemia 17 Edema is one of the most important of these. Hachinski et al 18 found decreased levels of HVA in lumbar CSF of patients with brainstem infarcts.…”

Section: Discussionmentioning

confidence: 99%

“…Previous reports of patients with stroke have not specified the type of lesion, the vascular territory, 17 or the entity of edema, 17 l8 evaluated either directly by CT scan or indirectly by the degree of impairment of consciousness, EEG, or angiography.…”

Section: Discussionmentioning

confidence: 99%

Homovanillic acid and 5-hydroxyindoleacetic acid modifications in CSF of patients with stroke and multi-infarct dementia.

Smirne

Franceschi

Truci³

et al. 1985

Stroke

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1003SUMMARY Thirty four patients who had complete ischemic stroke confirmed by neurologic examination, were divided into three groups according to the time elapsed between the first signs of stroke and lumbar puncture: group A, 22-47 h; group B, 48-71 h; group C, 72-96 h. Nineteen patients with multiinfarct dementia (MID) assessed by neurologic and neurophysiologic examinations were also studied. The severity of the neurological deficit was assessed by the Norris rating scale. Nine age-matched subjects without neurologic disease served as controls. Levels of homovanillic acid (HVA) and 5-hydroxyindolacetic acid (5-HIAA) were determined in lumbar CSF by a fluorimetric method after separation on Sephadex G-10 columns. HVA levels decreased as the length of time after stroke increased and were lower than controls in MID, while 5-HIAA levels were low in group B and MID. Our results in stroke can be interpreted as showing they are the consequence of dopamine and serotonin global depletion in the early phases of brain ischemia. In MID, the CSF changes might reflect not only tissue loss secondary to multiple infarcts but also the persistence of a state of diffuse ischemia. Stroke Vol 16, No 6, 1985 ALTERATIONS OF neurotransmitter functions in cerebral ischemia and stroke have recently received increasing attention. Studies in various animal species have shown that catecholamine (CA), serotonin 5-HT) and amino acid (AA) biosynthesis in brain is dependent on arterial and tissue pO 2 .' Severe ischemic conditions with derangement of the cerebral energy state markedly reduce monoamine and protein biosynthesis 2 " 5 with depletion of noradrenaline (NA), dopamine (DA) and 5-HT and reduction of AA metabolism.2 " 8 After severe unilateral ischemia these modifications are present not only in the damaged tissue but also in remote "non-ischemic" areas and in the controlateral hemisphere.3 -9 " 12 In the post-ischemic phase the main metabolite of DA, homovanillic acid (HVA) and of 5-HT, 5-hydroxyindoleacetic acid (5-HIAA), accumulate in the damaged tissue and in the adjacent edema zone. 4 -10 Human post-mortem studies confirmed the findings in animal models. After recent brain infarct severe depletion of CA, 5-HT and their metabolites was found in necrotic and intact areas. 13 In older brain infarcts a reduction of 5-HT and 5-HIAA was still present in necrotic tissue while adjacent tissues showed almost normal levels indicating some recovery. 13Thus, both animal and human studies have shown that marked changes of neurotransmitter metabolism occur in ischemic brain tissue and that these changes may have a complex time pattern. It therefore appears important for the understanding of the relationships between ischemia and neuron function to study the temporal profile of neurochemical changes in the ischemic brain. In patients this can only be accomFrom the Department of Neurology, Instituto Scientifico San Raffaele, and the Department of Pharmacology, Medical School, Universita' Degli Studi, Milan, Italy.Address correspondence t...

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ABSTFiAm -Twenty-one patients with acute brain infarction, 8 with transient ischemic attack and 20 controls were investigated for lumbar cerebrospinal fluid (CSF) monoamine metabolites and cholinesterases. The diseased patients were lumbar punctured on 2 occasions, mean Days 1 (0-3) and 5 (3)(4)(5)(6)(7)(8)(9) after debut of symptoms. Monoamine concentrations were Controls n = 20 Sex: Age (Mean f S.D.

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confidence: 99%

Increased monoamine metabolite concentrations and cholinesterase activities in cerebrospinal fluid of patients with acute stroke

Wester

Puu

Reiz

et al. 1987

Acta Neurologica Scandinavica

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Twenty-one patients with acute brain infarction, 8 with transient ischemic attack and 20 controls were investigated for lumbar cerebrospinal fluid (CSF) monoamine metabolites and cholinesterases. The diseased patients were lumbar punctured on 2 occasions, mean Days 1 (0-3) and 5 (3-9) after debut of symptoms. Monoamine concentrations were determined by reverse phase liquid chromatography with electrochemical detection and the cholinergic enzymes were measured photometrically. Increased concentrations of 3-methoxytyramine (3-MT), homovanillic acid (HVA), 5-hydroxyindoleacetic acid (5-HI-AA) and increased activity of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) in lumbar cerebrospinal fluid was found in patients with acute brain infarction when compared to control values, while the levels of 3-methoxy-4-hydroxyphenylglycol (MHPG) were not altered. No change of any neurotransmitter metabolite concentration/enzyme activity were found between Day 1 and Day 5 in the diseased patients. These data suggest an increased release of these neurotransmitter markers from necrotic brain areas into the cerebrospinal fluid and/or altered barriers between blood, brain and CSF and/or a dysfunction of the arachnoid villi to clear substances from the CSF. We therefore concluded that CSF neurotransmitters may be useful as specific brain markers in acute stroke.

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Neurochemical Alterations in Cerebrospinal Fluid in Cerebral Ischemia and Stroke

Cited by 8 publications

References 41 publications

Excitatory amino acids in the cerebrospinal fluid of asphyxiated infants: relationship to hypoxic‐ischemic encephalopathy

Excitatory amino acids in the cerebrospinal fluid of asphyxiated infants: relationship to hypoxic‐ischemic encephalopathy

Homovanillic acid and 5-hydroxyindoleacetic acid modifications in CSF of patients with stroke and multi-infarct dementia.

Increased monoamine metabolite concentrations and cholinesterase activities in cerebrospinal fluid of patients with acute stroke

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