Neurotransmission after a Brain Injury

Neurotransmission gets altered after a brain injury. The causes for this are multifaceted and include; mitochondrial dysfunction, axonal dysfunction, and changes in ion flux. 

Axonal Stretch

Axons, nerve fibers that conduct electrical impulses, are vulnerable to any biomechanical stretch. Axonal Stretch occurs with any direct hit to the head or body. The brain floats freely in fluid contained inside the skull. Because of that floating, hits of almost velocity cause the brain to slosh into the skull walls. This causes nerve impulses to slow or even disconnect completely, leading to cognitive symptoms including; learning and memory challenges, brain fog, and headaches. Axonal stretch can lead to atrophy and shrinkage of the neuron. Sometimes, these neurons become permanently damaged. If a neuron is permanently damaged, it can not recover normal nerve function. 

Unmyelinated nerve fibers, the sheath that increases nerve impulses, are very vulnerable to biomechanical stress. This leads to concerns with younger brains. Younger people have more white matter where the unmyelinated neurons are located. 

Ion Channel Dysfunction

After a head injury, impacts to the ion gated channels in the neurons shift the Glutamate (excitatory) and GABA (inhibitory) balance. Increases in Glutamate lead to high levels of calcium in the cell. The higher calcium levels lower the threshold for the nerves to fire leading to heightened states of anxiety, panic, and PTSD. 

So how do we get our neurons back to baseline? 

• Address high glutamate and calcium levels by giving oral or IV Magnesium

• Lithium orotate can help balance that dopamine neurotransmission 

• L-theanine to increase GABA levels and reduce anxiety 

• Progesterone acts to induce GABA, which can help to reduce anxiety

• Fish Oil is shown to decrease axonal damage
  
  PMID: 12937489, 29699444, 30666088, 16930802, 31198800