The Role Of The Brain Structures In Behaviour
The brain, undoubtably the most complex biological machinery known to our current universal understanding (Huang and Luo, 2015). This remarkably intricate system reflects its complexity in the fact that it attempts to comprehend itself. Its complex nature transcends any current technology and subsequently, limits our ability to develop a complete interpretation of this system. However, technological advancements and innovative research have granted us a greater understanding of how the brain coordinates its activity; furthermore, enabling us to construct structure-function relationships (Huang and Luo, 2015). These relationships are crucial to our understanding of brain-damage related diseases and injuries. One aspect of the brain that can be damaged as a result of Traumatic Brain Injury (TBI) is behaviour and emotion (McKee and Daneshvar, 2015).
Behavioural Anatomy
Protected by several layers, including the skull and meninges (dura mater, pia mater, and arachnoid mater) the brain is comprised of three fundamental parts: the forebrain, midbrain and hindbrain. The forebrain consists of the cerebrum, hypothalamus, and thalamus. The midbrain features the tectum and tegmentum. Whereas, the pons, medulla and cerebellum construct the hindbrain (Bear, Connors and Paradiso, 2015). Figure 1 presents the lobes of the brain, brain structural surface anatomy, and the medial surface of the brain.
‘Mechanism of Emotion’ – James Papez, 1937First coined in 1937, the Papez circuit, later to be known as the limbic system is a functional concept that describes the interconnected relationships between brain structures in the control of innate behaviours and basic drives of emotion (Rajmohan and Mohandas, 2007). This ‘proposed mechanism of emotion’ identifies several brain structures, that have been evidenced as essential to behavioural regulation. These include: the olfactory bulb, the hippocampus and parahippocampal gyrus, the cingulate gyrus, the fornix, the hypothalamus and thalamus, and the amygdale, to name a few (Sokolowski and Corbin, 2012). This subcortical system is also closely connected to the prefrontal cortex (PFC) and basal ganglia by neural circuitry (Rajmohan and Mohandas, 2007). In addition to emotion control, the system operates via influencing the endocrine and autonomic nervous system (ANS) in processes such as: motivation, time perception, consciousness, memory, attention, instincts, and sensory processing (Sokolowski and Corbin, 2012). Damage to limbic system structures or disruptions in circuits can result in cognitive, personality and behavioural defects, due to alterations in the structures that facilitate these survival factors (McAllister, 2011).
The Case Specifics
As depicted in the case study, a 45-year-old university professor, Dr C, received a severe head injury while mountaineering. This injury caused by an ice axe falling and striking Dr C, causing a depressed fracture of the frontal bone, and an initial loss of consciousness. This type of injury is classed as a TBI. TBIs elicit a range of characteristic damages that can be highlighted via MRI. However, the determining factors of brain-damage severity are the force of impact, the location of the damage (primary and secondary damage) and the timely management of treatment (Ahmad et al. , 2018). Primary TBI damage, occurs at the time of the event, where brain tissue (neurons, glial cells, and endothelial cells) is destroyed upon impact (Reis et al. , 2017). Whereas, secondary damage, including raised intercranial pressure and ischaemia, is a resultant of the initial injury; therefore, damage develops over a variable time period. Furthermore, damages can be categories into diffuse and focal injuries (McKee and Daneshvar, 2015). Cell damage responses include necrosis and apoptosis (McAllister, 2011). Figure 2, presents MRI imaging, comparing MRI that is consistent with TBIs from frontal bone localised depressed skull fractures (DSFs) and MRI from an individual with no brain injuries ((Szczepanski and Knight, 2014). It can be inferred from the case study and the MRI that Dr C has experienced a TBI; primarily, frontal lobe localised damage, due to a DSF. Information given regarding his recovery and progressive health state can be used to identify possible damaged brain structures.
Predominately, DSFs are seen to impact the frontoparietal region as the thin frontal bone is prone to trauma (Ahmad et al. , 2018). The resultant of which typically promotes alterations in personality, emotion and cognition (McAllister, 2011). The symptoms presented in Dr C’s case are also prevalent in the famous neurological patient, Phineas Gage, who developed cognitive and behavioural alterations, in consequence to PFC damage caused by a penetrating foreign object (Damasio et al. , 1994). In alignment with this, both case individuals appeared to make an initial full recovery, with no motor, sensory, or cognitive abnormalities. This is a frequently observed characteristic of TBI (Van Horn et al. , 2012). However, secondary damage typically exacerbates and becomes eminent as time proceeds (McAllister, 2011). Prefrontal Cortex (PFC) - Cognition and Personality Changes One structure that is particularly susceptible to damage from TBIs is the PFC. Part of a three-part frontal cortex system, the PFC functions in executive cognition, alongside the orbitofrontal cortex and medial frontal cortex, that have individual roles and subdivisions (McAllister, 2011). Damage to the dorsolateral PFC and subcortical white matter connecting the regions may be responsible for the behavioural changes profiled by Dr C (McAllister, 2011). Numerous responses to damage lead to atrophy, necrosis and apoptosis in affected area (e. g. neuron cell death), which can result in faulty connections within system neural circuits (McAllister, 2011). Lesions of the anterior cingulate cortex (ACC) would explain some of the defects that Dr C has been displaying. In particular, the lack of direction in planning and monitoring of errors within his lectures is a distinct characteristic of ACC atrophy (McKee and Daneshvar, 2015).
As well as direct primary damage, Dr C experienced a loss of consciousness from concussive force. This force dependant loss of consciousness can, in itself, cause long-term damage of the brain (McKee and Daneshvar, 2015). Shockwaves propagate through the brain, resulting in the deformation of brain tissue (blood-vessels, neurons, glial cells, and membranes). Vulnerable to this, axons can be destroyed which can disrupt the frontal-subcortical circuits; thus, creating faults between connecting structures. This damage is known as diffuse axonal injury (DAI), and has been shown in prelimbic cortex (PL)-amygdalae circuit damage, as the downstream effects modulate the activity of the amygdalae (McAllister, 2011; Rhodes and Murray, 2013). Therefore, the normal functions of anger-fear control are altered and there is an upregulation in anger expression (Rhodes and Murray, 2013). This could be a possible explanation for the aggressive responses detailed in the case. Alternatively, this factor could have been manifested from force-dependant hematoma or haemorrhage. The most common TBI-induced damage, of this kind, is subarachnoid haemorrhages, which is bleeding in the subarachnoid space. When the fictitious force (acceleration-deceleration) exceeds the tolerance of the brain tissue, the pressure inside bridging veins exceeds the compliance tolerance of venous membranes; thus, ruptures occurs (McAllister, 2011). The delayed behaviour changes, elicited by Dr C, may be a result of the slow accumulation of the subsequent haemorrhage. Clinically, the symptoms can be delayed hours or days after the initial injury (Harvey and Close, 2012).
In a paper by Chow (2000), post-concussion disorder is shown to present many of Dr C’s behavioural changes, including: social inappropriateness, irritability and aggressive responses, apathy, and emotional lability. Reflecting on the symptoms presented, it is unlikely that the acceleration-deceleration forces involved damaged any motor centres, as no motor alterations were displayed. Thereby, it can be postulated that, the diffuse damage did not extend to the right ventrolateral PFC, as this structure ordinarily functions in motor inhibition and reflexive reorienting (Levy and Wagner, 2011). TBIs have also been shown to promote the accumulation of numerous neurodegenerative-related proteins, including β-amyloid, a marker for Alzheimer’s disease (AD) (McKee and Daneshvar, 2015). This knowledge considered, it can be suggested that Dr C is more susceptible to developing this neurodegenerative disease. Orbitofrontal cortex (OFC) - Social Behaviour Changes Orbitofrontal cortex (OFC), an area of critical social comportment is also vulnerable to the effects of TBIs. Neurotrauma of this nature can cause a disruption in the frontal-subcortical circuits and as a result, individuals are likely to form patterns of disinhibited behaviours (McAllister, 2011).
The OFC plays a vital role in intuitive reflexive social behaviours; thus, the individual may make decisions in a social situation, that do not conform to the ordinary expected rewards/punishments of that given action. Some progressive cognitive states, presented by Dr C, correlate to those associated with OFC degradation, including: poor judgement of social interactions, a tendency to make inappropriate remarks or take unreasonable action in social situations (as mentioned above), and poor empathising ability (Schoenbaum et al. , 2011). These symptoms are well-established in the case of Phineas Gage (Damasio et al. , 1994). The degeneration of OFC has also been linked to some forms of frontotemporal dementia (McAllister, 2011). Considering this and the behaviour deterioration described in the study, it is probable that Dr C will develop a neurodegenerative disorder.
Amygdalae - Aggression In the study, Dr C is reported to have sudden outbursts of temper. This increased propensity in failing to regulate negative emotion (e. g. agitation/aggression) is likely to be a result of structural abnormalities in the brain region(s) or connections, that regulate anger (Rajmohan and Mohandas, 2007). One of these structures is the amygdalae. In addition to functioning in emotional responses, the amygdalae also play a primary role in decision-making and memory. The structure receives and transmits threatening environmental stimuli to the basal ganglia and onwards to other connecting centres (McAllister, 2011). It is far more likely that, in Dr C’s case, primary brain injuries have been the resultant of amygdalae alterations.
For example, bone fragments could have caused damage to the PFC and OFC, just two of the structures that modulate the activity of the amygdalae, through inhibition (Davidson, Putnam and Larson, 2000). In this case, it is unreasonable to suggest the bilateral destruction of the amygdalae or any lesion damage, as Dr C would present placidity (Rajmohan and Mohandas, 2007). Interestingly, Gage’s skull revealed a prominent correlation between OFC-amydalae-linked damage and emotion-related abnormalities, which have been evidenced in both animal models and humans (Damasio et al. , 1994). In TBIs, it is typical to see neurotransmitter system damage, particularly cholinergic and catecholaminergic. Both systems are essential in behavioural homeostasis and the regulation of emotions (McAllister, 2011). Serotonin is the most researched neurotransmitter in aggression-related disorders; with serotonin imbalance treatments, such as: beta-blockers (propranolol and pindolol), as the leading interventions for these disorders (Warden et al. , 2006).
TBI-Related Disorders: Effect on Brain Physiology and Behaviour Table 1: TBI-Related brain disorders. Conclusion Reflecting on the case, it can be determined that not all frontal lobe TBIs present the same characteristics of severity. From Phineas Gage to Dr C differences and similarities can be drawn. In this case, we have highlighted some of the potential brain injuries, that could explain the symptoms that Dr C is presenting, relating this to their structure and function. However, this deduction is complicated when faced with the fact that the regulation of emotions has a limitless variety in the stimuli that can affect the emotional brain (Bear, Connors and Paradiso, 2015). There is still much needed progress in this area of study. Once conversely described as a singular control of emotion, developing from James-Lange theory and Cannon-Bard theory to the multidimensional, multifactorial control of emotions that we accept today, the future is still open to a greater understanding of what makes us human (Huang and Luo, 2015).
