Understanding Brain Trauma and Neuroplasticity

In December of 1993, former World Boxing Champion John Famechon (who had sustained severe incapacitating brain injuries in August 1991) began a new, complex multi-movement therapy and rehabilitation program, which eventually helped him regain a condition close to his pre-accident state. What was of particular interest to Professor Ken Purnell (in relation to the self-evident presenting recovery behaviour of John Famechon), was the process of discovering (especially at the neurological level); what was involved in changing John’s presenting physical condition (that of being incapacitated for 28 months), to where John had recovered to a presenting behaviour condition, that was now close to what existed prior to his accident (K. Purnell, personal communication, April 24, 2015).

The Start of Unpacking the Research Dealing with Brain Trauma

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Unpacking the Research Dealing with Brain Trauma

When brain trauma takes place, research informs there is an instant inherent response (“by the brain” to this trauma) through a wide variety of means. All of this has only one purpose: to commence an immediate repair of all of the damaged parts of the brain. The neurobiological and neurophysiological function of this, is to lead to an immediate brain recovery condition (and the commencement of the return of homeostasis) that existed prior to when the brain trauma occurred.

Homeostatic Self-regulation

All of this is powerfully captured by Doidge (2015), who writes: “Homeostatic self-regulation isn’t just one thing among others that living things do. Self-regulation, maintaining order within chaos, is the essence of life … Thus, self-regulation – the cure through finding homeostasis – is so welcome, so familiar, and so appealing because it is not something we can do only sometimes; it is as long as we are healthy and alive, what we are always doing.” If this were not the case with regard to brain plasticity, it is unlikely that John Famechon would ever have recovered.

Brain Plasticity Research

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Defining Brain Plasticity

The importance of brain plasticity is strongly emphasised by Doidge (2010a), who has been recorded as stating that the discovery and the actuality of brain plasticity is “one of the most extraordinary discoveries of the twentieth century” (K. Purnell, personal communication, November 27, 2014).

There are a variety of other definitions of brain plasticity. Doidge (2010) contends that brain plasticity refers to the brain being “changeable, malleable, modifiable.” Kolb, Muhammad and Gibb (2011) define brain plasticity as “the capacity of the nervous system to change its structure and ultimately its function over a lifetime.

The definition of neuroplasticity by Ormerod and Galea (2012) could be described as being specific to John’s circumstance. That is because their definition states that learning and the environment have an impact on changing the brain. They point out that learning and the external environment influence the brain, where changes begin to occur in a cell or a group of cells, which cascades to extracellular changes.

According to Ormerod and Galea (2012), this cascading process causes: “modifications in electrophysiological properties, receptor number or sensitivity, synapse number, and cell number that either independently or interdependently alter cell signaling. Events that precipitate neuroplasticity can be environmental (learning, repeated stress, or enriched housing) or hormonal in nature. Neuroplasticity, in turn, permits us to incorporate experience into adaptive response to our environment.”

Inherent Neurological Repair Mechanisms Following Brain Injury

The research in the field of acquired brain injury and brain plasticity has found that internal neurological and neurophysiological recovery (collateral sprouting) commences at the very instant a trauma to the brain is acquired, irrespective of whether the injury has occurred as the result of an internal condition (such as a stroke) or an external condition (Esty & Shifflett, 2014; Goodrich et al., 2014).

When any external application is applied (such as a medical intervention or any form of external rehabilitation), the internal neurological structures of the brain also respond to these external interventions by altering its neurological structures and functions (Devor, 1975; Doidge, 2010, 2015; Guth, 1969; Hunter, 1987; Kimble, 1992).

Neuroplasticity Essential Reads

Physical Activity Initiates An Immediate Response

Neurological Functions Associated with Acquired Brain Injury

The Neuro-manifestation of Collateral Sprouting

Glees and Cole (1950) and Lui and Chambers (1958) found evidence of immediate neuroplasticity response to an acquired brain injury as the result of an internal initiating process they referred to as collateral sprouting. Collateral sprouting is also known as new axon collaterals and axonal collateral sprouting.

Collateral sprouting is a process where new axons and/or neurological pathways begin to immediately sprout in response to an injury in the internal structures of the brain (Devor, 1975; Doidge, 2010; Glees & Cole, 1950; Guth, 1969; Hunter, 1987; Lui & Chambers, 1958; Luria, 1964).

Further to this, Merzenich et al. (1983) noted that when the brain is injured, it regenerates collateral axonal sprouts instantly close to and/or immediately to where the injury occurred. This neurophysiological phenomenon attempts to re-establish new axonal, dendritic, and new synaptic connections (synaptogenesis) to bring about the same homeostatic brain functioning that existed before the onset of the injury (Devor, 1975; Doidge, 2010; Guth, 1969; Hunter, 1987; Kimble, 1992).

Synaptic Remodelling and Reactive Synaptogenesis

In their studies, Kalat (1992) and Kimble (1992) found that when brain trauma is experienced (in addition to the collateral sprouting), the septal nuclei initiate synaptic remodelling and reactive synaptogenesis. The septal nuclei are a group of cells found at the midline of the forebrain. This area serves as the main synaptic junction between the hippocampus and hypothalamus.

This process of synaptic remodelling and synaptogenesis helps with the brain’s dendritic connections and synaptic neurotransmissions (Hunter, 1987; Kalat, 1992; Kimble, 1992; Kolb, 1993; McGuigan, 1994; Nowakowski, 1993; Pinel, 1997; Rosenzweig et al., 1996). It also “leads the brain” to try to instantaneously re-establish the complex neurological structures and all of the complex networks that existed prior to the injury taking place.

The research informs that the neurophysiological purpose of this process (is to not only to counter the immediate neurological damage that had now taken place), but, importantly (and profoundly), to also restore – the brain, mind and body – to the same wholistic homeostatic performance condition, that existed prior to the accident and injury taking place. The research (that has now taken place, in relation to the recovery of John Famechon), strongly suggests that this internal brain-based neurological recovery process may have taken place with John Famechon.