Table 1.
Acute neurometabolic changes following mTBI
| Post-injury change | Mechanism | Pathophysiologic effect | Recovery timeline | |
|---|---|---|---|---|
| Glutamate | Immediate release from injured neurons followed by region-specific decrease | “Mechanoporation” produces neuronal depolarization and neurotransmitter release |
Promotes feedback loop of depolarization and neuron hyperexcitability Promotes influx of sodium and calcium |
Initial increase normalizes within minutes of injury Region-specific decrease at 72 h recovers by 2 weeks post-injury |
| Gamma-amino-butyric-acid (GABA) | Decreased in a region-specific and time-dependant manner | Loss of GABA-ergic interneurons has been suggested [14] | Decreased neuronal inhibitory effect | Region-specific decrease up to 2 weeks |
| Potassium | Extraneuronal increase | Glutamate stimulates potassium efflux via ligand-gated potassium channels | Stimulation of feedback loop of depolarization and hyperexcitability | Within 10 min from injury |
| Calcium | Intraneuronal increase/accumulation |
Initial neuronal “mechanoporation” Promoted by glutamate release |
Cell damage and mitochondrial impairment | Approximately 3 to 4 days after injury |
| Glucose | Increase followed by decrease | Increased neuronal glycolysis followed by hypometabolism + blood flow-uncoupling |
Decreased ATP from deficient oxidative metabolism Ineffective anaerobic metabolism |
Hyperglycolitic phase: • 30 min to 6 h Hypometabolic phase: • 5 to 10 days |
| Blood flow | Global as well as regional and time-dependant decreases |
Autoregulatory and vasoreactive disturbances induced by CO2 Local and diffuse structural vessel damage |
Promotes anaerobic metabolism “Window of vulnerability” to repeated head impacts |
Approximately 10 days |