Neurological Functions Associated with Acquired Brain Injury

Examining ABI recovery of John Famechon former World Boxing Champion

Source: Microsoft Copilot / Microsoft

In December 1993, former World Boxing Champion John Famechon, who had suffered a severe brain injury in August 1991, began participating in a new and novel multi-movement therapy that enabled him to return to a condition similar to what existed before his incapacitation.

Research indicates that following the onset of an acquired brain injury (ABI), the brain initiates an immediate neurobiological response to help restore the brain and body to the homeostatic state that existed prior to the ABI. This includes processes like that of collateral sprouting, synaptogenesis and neurogenesis.

The literature on acquired brain injury and associated internal brain-based repair and recovery research informs that the formation of new neurons (neurogenesis; new synapses (synaptogenesis); and related synaptic connections (all contribute to the expansion of neurotransmitter propagation), leading to the development more complex neurological and neurophysiological connections, which includes brain-derived neurotrophic factor (BDNF).

Brain derived neurotrophic factor (a secreted protein) is acknowledged for its role in promoting neurogenesis and, consequently, also facilitating neurological plasticity (Ding, Ying, & Gómez-Pinilla, 2011; Doidge, 2010; Doidge, 2015; Graczyk & Rickman, 2013; Jariel, 2013, Mannion et al., 1996; Roland, 2014; Ying et al., 2002).

Research has also found that neurogenesis (the formation of new neurons, along with associated neurological plasticity) can continue well into advanced adulthood; particularly when an external event occurs (such as engaging in regular physical activity for at least thirty minutes each day).

This extended process (in terms of time itself), which, as noted, also involves the ongoing development of new neurons into adulthood, is specifically referred to as adult neurogenesis (Abrous et al., 2013; Ming & Song, 2011; Ormerod & Galea, 2012; Suzuki, 2015). This research, therefore, strongly suggests that adult neurogenesis, alongside exercise, would have significantly influenced John’s recovery.

As such, it would be reasonable to infer that this new and novel complex multi-movement therapy (along with all of the medical interventions and associated medically directed physiotherapy that followed) would also have played a significant role in John’s recovery. I will now begin to explore further what else may have contributed to John’s condition, from being incapacitated for 28 months, to his presenting and ongoing recovery. This journey of discovery will commence with the associated examination of neurogenesis and Brain derived neurotrophic factor.

Examing the literature dealing with neurologial repair processes

Source: Microsoft Copilot / Microsoft

Brain derived neurotrophic factor (BDNF)

According to Arden (2010, italics in original), “[o]ne of the most important players in both neuroplasticity and neurogenesis is … brain-derived neurotrophic factor (BDNF).” In terms of its neurological and overall brain functioning importance, brain derived neurotrophic factor (BDNF) not only helps to propagate “and maintain the infrastructure of cell circuitry” (Arden, 2010). BDNF also helps to make active the genes that increase the production of even more brain derived neurotrophic factor proteins and also the neurotransmitter serotonin (Arden, 2010, Suzuki, 2015).

Brain derived neurotrophic factor also has the capacity to attach itself to synapse receptors. As a consequence of BDNF and synaptic receptor binding, this neurophysiological event results in the synapse being able to initiate a cascading flow of ions that leads to an increase in the transmission voltage at the synapse.

According to Arden (2010), this process helps to strengthen the connections “between the neurons,” which brings with it the physiological capacity that these neurons will now tend to fire together. In addition to this, brain-derived neurotrophic factor is also indirectly activated by the excitatory neurotransmitter glutamate. This action helps to increase the production of protective proteins and also that of internal antioxidants.

The research indicates that these internal antioxidants are able to provide protective physiological qualities. There needs to be a balance in the body between free radicals and antioxidants. This balance is crucial because it helps to bring about beneficial physiological functions. Free radicals, for example, have the potential to bring about a condition referred to as oxidative stress.

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Oxidative stress can adversely alter the cell function of proteins, lipids, and even DNA, which can lead to illness and disease. The consumption of external sources of antioxidants is thought to be able to assist in reducing the negative effects that free radicals and oxidative stress produce (Lobo, Patil, Phatak, & Chandra, 2010).

There are two types of vitamins that areable to combat the adverse biological effects of free radicals and oxidative stress. These are the antioxidants vitamin C, and vitamin E. Vitamin C is necessary to manufacture noradrenaline/norepinephrine. According to Arden (2010), “[v]itamin C is one of the principal antioxidants and acts as a scavenger of free radicals,” and vitamin E is reported to be beneficial for blood vessels.

Further to the protective features provided by brain derived neurotrophic factor, the research has found that the release of BDNF helps cells to enhance their growth and increase their active longevity (Arden, 2010; Doidge, 2015). Added to this is the knowledge that exercise helps to increase the release and activation potential of brain derived trophic factor (Arden, 2010; Doidge, 2010; Doidge, 2015; Suzuki, 2015).