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
Published online Feb 26, 2017. doi: 10.4331/wjbc.v8.i1.21
Structure effected | Findings in brain injury | ||
Cerebro spinal fluid | Blood/serum | ||
Tau protein | Axon | Levels peak 4-8 d after injury[111,112] | Elevated levels in hypoxic injury[113,114] |
Myelin basic protein | Axon | Precise measurement difficult[115] | Elevated levels in brain injury[116] |
γ-enolase | Neuron | Confounded 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 β | Astrolglial cells | Elevated levels but less sensitive[108] | Confounded by release from extracerebral tissue[118] |
GFAP | Astroglial cells | Elevated levels but less sensitive[107,108] | Serum levels correlate with changes in brain imaging[119], no extracerebral sources detected[120] |
UCH-L1 | Neuron | NA | Only one pilot study[98] |
Variable | Normal levels (at a flow rate of 0.3 μL/min) | Clinical implications |
Lactate | 2.9 ± 0.9 mmol/L | Increased levels seen in ischemia and hyperglycolysis[121-123] |
Pyruvate | 166 ± 47 μmol/L | Decreased levels seen in ischemia and hypoxic conditions[124,125] |
L/P ratio | Normal value-20 | Value > 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] | ||
Glycerol | 82 ± 4 μmol/L | One of the constituents of the cell membranes |
An increase in levels signifies cell damage[124] | ||
Glutamate | 16 ± 16 μmol/L | Marker of excitotoxicity[124] |
Glucose | 1.7 ± 0.9 mmol/L | Changes in blood flow or metabolism cause disproportionate changes in brain glucose |
Affected by ischaemia, hyperaemia, hyperglycaemia, hypermetabolism and hypometabolism[124] |
Clinical condition | CMD implications |
Traumatic brain injury | Helpful 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 haemorrhage | Detection 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 stroke | Detecting development of oedema of the infarcted tissue[141] |
Monitoring effects of decompression hemicraniectomy and hypothermia in stroke patients[142,143] | |
Brain tumours | Neurobiochemistry 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] | |
Epilepsy | Study of biochemical milieu of epileptic focus[149] |
Other applications | Study 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 |
- Citation: Sahu S, Nag DS, Swain A, Samaddar DP. Biochemical changes in the injured brain. World J Biol Chem 2017; 8(1): 21-31
- URL: https://www.wjgnet.com/1949-8454/full/v8/i1/21.htm
- DOI: https://dx.doi.org/10.4331/wjbc.v8.i1.21