Abstract
The authors are aware of only one article investigating amino acid concentrations in cerebrospinal fluid (CSF) in patients with ruptured intracranial aneurysms, and this was published 31 years ago. Since then, both management of subarachnoid haemorrhage (SAH) and amino acid assay techniques have seen radical alterations, yet the pathophysiology of SAH remains unclear. To analyse the pattern of concentrations of amino acids and related compounds in patients with different outcomes following aneurysmal SAH. 49 CSF samples were collected from 23 patients on days 0-3, 5, and 10 post-SAH. Concentrations of 33 amino acids and related compounds were assayed by liquid chromatography tandem mass spectrometry in patients with good [Glasgow Outcome Scale (GOS) 1-3] and poor (GOS 4-5) outcome. Of the 33 compounds assayed, only hydroxyproline and 3-aminoisobutyric acid appeared not to increase significantly following SAH. In poor outcome patients, we found significantly higher concentrations of aspartic acid (p = 0.038), glutamic acid (p = 0.038), and seven other compounds on days 0-3 post-SAH; glutamic acid (p = 0.041) on day 5 post-SAH, and 2-aminoadipic acid (p = 0.033) on day 10 post-SAH. The most significant correlation with GOS at 3 months was found for aminoadipic acid on day 10 post-SAH (cc = -0.81). Aneurysmal rupture leads to a generalised increase of amino acids and related compounds in CSF. The patterns differ between good and poor outcome cases. Increased excitatory amino acids are strongly indicative of poor outcome.
Highlights
Subarachnoid hemorrhage (SAH) due to ruptured intracranial aneurysms is a life-threatening condition with an annual incidence of 2–22.5/100,000 population per annum
The concentrations of the 33 compounds were established for 49 samples derived from 23 SAH patients (Table 1), and 25 samples collected from 25 control patients
Rupture of an aneurysm led to a significant elevation of 27 of the 33 compounds in the cerebrospinal fluid (CSF) at days 0–3 post-SAH (Table 2)
Summary
Subarachnoid hemorrhage (SAH) due to ruptured intracranial aneurysms is a life-threatening condition with an annual incidence of 2–22.5/100,000 population per annum. During EBI, the central nervous system (CNS) suffers from “primary” insults (involving acute changes of intracranial pressure, cerebral perfusion pressure, and cerebral blood flow with vascular constriction and obstruction of the microcirculation), and “secondary” ischaemic processes (including anaerobic cellular respiration, energy depletion, impaired protein synthesis, excitotoxicity, free radical attack, neuronal stress, and DNA damage, leading to apoptosis and necrosis) [16] Many of these processes may potentially be initiated, mediated, or terminated by amino acids and related compounds. The authors are aware of only one article investigating amino acid concentrations in cerebrospinal fluid (CSF) in patients with ruptured intracranial aneurysms, and this was published 31 years ago Since both management of subarachnoid haemorrhage (SAH) and amino acid assay techniques have seen radical alterations, yet the pathophysiology of SAH remains unclear
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