Case of Phineas Gage Revisited

As far as is known to date, the importance of executive functions (EFs) in our lives was of immense interest over the last centuries. EFs will appear in almost every moment of our lives where our brains require cognitive control (e.g., crossing streets, restraining anger, reasoning conversations, solving math calculations, etc.). Considering all these vital life skills, EFs can be described as a great number of cognitive capabilities coordinating to sustain human cognition whilst helping initiation/inhibition of behaviour, shifting attention and being cognitively flexible, making decisions, planning, self-regulation. Plainly, ‘Executive function is an overarching term that refers to mental control processes that enable physical, cognitive, and emotional self-control.’ (Corbett et al., 2009, p. 210). Elliott (2003) considers executive functions as a complex non-unitary term. Executive functions are mediated within the most anterior part of the brain, called prefrontal cortex; and this area accounts for 29% of the cerebral cortex (Fuster, 1995). Nowadays, neuroscientists are capable of distinguishing three key concepts of executive control; attention shifting, response inhibition, and working memory (Miyake et al., 2000).

 

Before scientists became curious about the contribution of this large area to human behaviour in the 1950s, the field of neuroscience witnessed the well-known incidence of Phineas Gage in 1848 (Harlow, 1999). The literature reveals that this case was a historic milestone in understanding executive deficits (Harlow, 1999; Goldstein et al. 2014). Phineas Gage numinously survived after an iron rod pierced into his forehead at a construction site, this event later on turned him into an unbearable person as his milieu described; he became unable to inhibit behaviours in a way that his lack of executive control and impulsivity led to an absence of self-regulation, being disinhibited and having completely changed personality after the injury (Harlow, 1999). Such dysfunction in executive control is a significant indicator for many neurological and psychiatric disorders (for the list of dysexecutive conditions, see Rabinovici et al., 2015). EMs may covertly affect obesity, schizophrenia, depression, obsessions and addictions as well as academic—difficulties in reading and writing—and marital problems; and, can be observed in many well-known conditions (Lezak, 1982; Pennington & Ozonoff, 1996; Harlow, 1999).

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Term of ‘executive malfunctions (EMs)’, was coined usually to point out prefrontal lesions (Stuss et al., 2011). EMs imply the absence of particular cognitive abilities. One of the most ubiquitous lesion-related malfunction is seen as lack of response inhibition (Baddeley, 1986; Norman & Shallice, 1986). Emerging with the case of Phineas Gage, scientists now believe that intact executive skills rely not only on the prefrontal area but also on the parietal, cerebellum, striatum, thalamus, and basal ganglia (Pennington & Ozonoff, 1996; Elliott, 2003; Schweizer et al., 2008; Brunamonti et al., 2014; Rabinovici et al., 2015). Nevertheless, the occipital region was found not to be correlated with EFs (Nowrangi et al., 2014). It is surprising that frontal damage do not guarantee worsening in executive skills; in the meantime, non-frontal damage can cause executive deficits as well (Mountain & SnowWilliam, 1993; Pennington & Ozonoff, 1996; Cowey & Green, 1996). EMs mostly promise lesions along with deformation in neurotransmission and white matter integration which may occupy different cortical and subcortical structures in various neurological and psychological conditions (Nowrangi et al., 2014). In line with this, there is a telling evidence of personality changes occurring after ventromedial frontal damage (e.g. Phineas Gage; Lezak, 1983; Miyake et al., 2000; Jose et al., 2020). Neuroscientists seemed to agree that whole conceptualisation and research of executive functions stemmed from patients with frontal lobe lesions (Damasio, 1979; Lezak, 1982; Miyake et al., 2000). To support the case of Phineas Gage, Rodríguez-Bailón et al. (2012) show that personality changes (e.g. being disinhibited and impulsive) are valid in patients with frontal damage. Scientists believe that lesions in ventromedial prefrontal cortex (VMPFC) can breed certain impairments in personality, motivation, risk-taking, social, emotional and behavioural disregulation (Lezak, 1982; Stuss, 2011). In a review on focal prefrontal lesions, Jose et al. (2020) conclude that the VMPFC facilitates decision-making, emotions and motivations whereas the dorsolateral prefrontal cortex (DLPFC) runs visuospatial and even more complex abilities. In Somatic Marker Hypothesis, Damasio (1995) discussed that such VMPFC damage will impair emotional and behavioural processes, especially decisionmaking. He claimed that emotions are controlled by the prefrontal area, along with the help of subcortical areas (amygdala, thalamus, hypothalamus). Therefore, Damasio (1995) inferred that patients with VMPFC lesion will have difficulties pairing their emotions and behaviours. Over and above, Chan et al. (2008) argued on two kinds of EFs; (1) hot EFs—directed by VMPFC which allows emotional and behavioural interactions in the social context, and (2) cold EFs—mediated by DLPFC which covers planning, reasoning and problem-solving. Also from an evolutionary perspective, Ardila (2008) pointed out two types of EFs; (1) metacognitive, (2) emotional & motivational. These EFs were also known with their syndromes—(1) dorsolateral and (2) orbitofrontal/ventromedial syndrome—if there is any lesion. The idea behind this surprisingly relates to hot and cold EFs. In addition, hot EFs or ventromedial syndrome can affect personality, impulsivity, mood changes, distractibility, general social intelligence (Fuster, 1989; Stuss et al., 2002; Rodríguez-Bailón et al., 2012). Nevertheless, none of prefrontal lesions certainly promise a lack of intelligence (Friedman et al., 2006). It is now well-understood that Phineas Gage did not show any meta-cognitive dysfunctions; however, his personality and motivation behind his behaviours were affected (see Harlow, 1999). On the other hand, Pennington & Ozonoff (1996) also suggest that one will become ‘euphoric’ (Fuster,1989) or ‘pseudo-psychopathic’ (Stuss & Benson, 1986) after orbitofrontal lesions. They further claimed that a patient would pay no attention to social norms and rules, and act disinhibited, facetious towards others (e.g. Conduct Disorder, Tourette Syndrome, Attention-Deficit Hyperactivity Disorder, Autism; Corbett et al. 2009). 

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Regardless of the timeline, there seems to be a notable consensus on personality changes occurring after frontal lesions (Damasio, 1979; Lezak, 1983; Miyake et al., 2000; Jose et al., 2020). On a brighter note, it now seems conspicuous that research in EFs has fostered the conceptualisation of lesion-related personality changes and their wide-ranging disturbances.

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