What Happens Inside The Head Following MTBI?

It is known that CT scans following MTBI are usually normal. However, studies using advanced neuro-imaging techniques (fMRI, MRI, SPECT, PET) have found such structural abnormalities as white-matter lesions at the center of each cerebral hemisphere. These findings argue the case that (1) neurologically-based behavioral deficits from MTBI do occur and (2) this population should not be excluded on the grounds of neuroradiological findings alone.

Recent studies have shown that a complex chemical cascade of biochemical and physiological events occur during the first minutes post-trauma. The traumatized area has a shut-down, or decrease in cerebral blood flow (CBF) to brain cells (neurons) followed by an increased demand for glucose, which in not present in sufficient amounts to maintain neuronal stability. The deficient blood supply (ischemia) combined with a deficient oxygen supply (hypoxia) leads to a metabolic disturbance with an immediate release of excitatory neurotransmitters (glutamate) that literally causes neurons to fire repeatedly (over-excite) until they die.

Minute, but significant damage may occur when the mechanism or force of injury leads to stretching and shearing of axons. Damage can occur in the brainstem along the (1) the Ascending Reticular Activating System (ARAS), which is critical for arousal and attention and (2) at the level of the pons, which is significant to the vestibular-system connections into the cerebral cortex. Concussive forces from a blow to the head or exposure to an explosion can lead to significant cochlea and/or vestibular system damage.

Proper identification of the above underlying causes helps clinicians to prescribe appropriate treatment. For example, such symptoms as fatigue, headache, and dizziness have many, varying causes, which need to be correctly identified.

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