Editorial
Copyright ©The Author(s) 2017.
World J Biol Chem. Feb 26, 2017; 8(1): 21-31
Published online Feb 26, 2017. doi: 10.4331/wjbc.v8.i1.21
Table 1 Serum and cerebrospinal fluid biomarkers of cerebral injury
Structure effectedFindings in brain injury
Cerebro spinal fluidBlood/serum
Tau proteinAxonLevels peak 4-8 d after injury[111,112]Elevated levels in hypoxic injury[113,114]
Myelin basic proteinAxonPrecise measurement difficult[115]Elevated levels in brain injury[116]
γ-enolaseNeuronConfounded by blood contaminated CSF[117]Serum levels are very sensitive to lysis of RBC in blood contaminated CSF[117], elevated levels in brain injury[116]
S-100 βAstrolglial cellsElevated levels but less sensitive[108]Confounded by release from extracerebral tissue[118]
GFAPAstroglial cellsElevated levels but less sensitive[107,108]Serum levels correlate with changes in brain imaging[119], no extracerebral sources detected[120]
UCH-L1NeuronNAOnly one pilot study[98]
Table 2 The components monitored by cerebral microdialysis and their clinical implications
VariableNormal levels (at a flow rate of 0.3 μL/min)Clinical implications
Lactate2.9 ± 0.9 mmol/LIncreased levels seen in ischemia and hyperglycolysis[121-123]
Pyruvate166 ± 47 μmol/LDecreased levels seen in ischemia and hypoxic conditions[124,125]
L/P ratioNormal value-20Value > 25 - metabolic crisis[124]
Type 1-lactate increased, pyruvate decreased, signifying ischemia
Type 2-raised LPR due to primarily decreased pyruvate level, seen in glycolysis failure or shunting of glucose to alternative metabolic pathways[125]
Glycerol82 ± 4 μmol/LOne of the constituents of the cell membranes
An increase in levels signifies cell damage[124]
Glutamate16 ± 16 μmol/LMarker of excitotoxicity[124]
Glucose1.7 ± 0.9 mmol/LChanges in blood flow or metabolism cause disproportionate changes in brain glucose
Affected by ischaemia, hyperaemia, hyperglycaemia, hypermetabolism and hypometabolism[124]
Table 3 Cerebral microdialysis implications in clinical scenarios
Clinical conditionCMD implications
Traumatic brain injuryHelpful in optimising therapy in neuro-ICUs as a component of multi-modality monitoring
Helpful in indivisualising management on the basis of cerebral perfusion pressure targets and assessment of response to medical and surgical interventions[126,127]
Predictor of severity, neurological outcome and long-term anatomical aberrations in the injured brain[128-130]
Detection and management of glycemic perturbations of the injured brain[131,132]
Predicting long-term anatomical alteration[133]
Subarachnoid haemorrhageDetection of ischemic changes during aneurysm clipping[134]
Specific for the detection of delayed ischaemic neurological deficit[135-138]
Prognostication of SAH patients[139,140]
Acute ischaemic strokeDetecting development of oedema of the infarcted tissue[141]
Monitoring effects of decompression hemicraniectomy and hypothermia in stroke patients[142,143]
Brain tumoursNeurobiochemistry of brain tumours[144,145]
Biochemical changes during treatment
Drug pharmacokinetics study[146]
Monitoring of drug effect
Development of tumor drug delivery systems[147,148]
EpilepsyStudy of biochemical milieu of epileptic focus[149]
Other applicationsStudy of the perihaemorrhagic zone in intracranial hemorrhage[150,151]
Study of biochemical changes and novel therapeutic options in neurodegenerative diseases such as Parkinson’s and Alzheimer’s disease