Does cerebral hyperglycaemia lead to activation of the neurotoxic polyol pathway?

Background:
Hyperglycaemia can lead to increased activity of the polyol pathway. In this pathway, glucose is metabolized to sorbitol and fructose. These metabolites are believed to be neurotoxic, however evidence on activation of the polyol pathway in the brain is scarce. Furthermore, activation of the polyol pathway could contribute to postoperative cognitive dysfunction (POCD). Both POCD as anaesthetic drugs (and surgical stress) are associated with hyperglycaemia.

Rationale:
We hypothesize that cerebral hyperglycaemia leads to activation of the neurotoxic polyol pathway and that increased activation of this pathway is associated with cognitive dysfunction

Study design:
Secondary analysis of data from a prospective cohort study

Methods:
Analysis of glucose, sorbitol and fructose will be performed on cerebrospinal fluid (CSF) of participants of the Anaesthetic Biobank of Cerebrospinal Fluid (ABC). Plasma glucose will also be analysed. In the ABC study, blood, CSF and clinical data are collected from patients undergoing spinal anaesthesia for elective surgery.

We hypothesize that cerebral hyperglycaemia leads to activation of the neurotoxic polyol pathway and that increased activation of this pathway is associated with cognitive dysfunction.

Time point 1: A neurological examination and Montreal Cognitive Assessment (MoCA) are performed pre-operatively.
Time point 2: CSF and blood are collected from adult patients undergoing spinal anaesthesia for elective surgery and stored.

Relevant clinical, surgical and anaesthetic data are registered.

None.