Psychopathy

Psychopathy is a mental disorder characterized by the absence of guilt and empathy in an individual. This disorder shows similarities to antisocial personality disorder ASPD and was officially recognized in 1968 when published in the Diagnostic and Statistical Manual of Mental Disorders, DSM-II. The limbic system is integral to the study of Psychopathy due to the reduction of functional connectivity in the Amygdala, Cingulate Cortex, and Ventromedial Prefrontal Cortex. Voxel and white matter integrity in the vmPFC-amygdala and UF respectively experience impaired associations, leading to abnormalities in judgment, fear, memory and distress causation [9] In addition to neuroanatomy, mutations in the MAOA gene (links between the 2R allele of the variable number tandem repeat area) increase the probability of violence, and assumed to be correlated with psychopathy[1]. Through current research analysis into Psychopathy allows us to transition from vague ideas from the early 60s to specific brain regions and pathways, aiding in the ability of treatment and prevention to be implemented. As greater knowledge is obtained, we can begin to identify risk factors, treatment, and removal of the negative stigma attached to a mental disorder of this caliber, thus allowing for seamless integration into society.

Psychopathy

Disorder

Psychopathy is a mental disorder characterized by the manifestation of unprincipled and antisocial behavior. Those diagnosed show the inability to love, and establish significant relationships. They are incapable of learning from previous experiences, and demonstrate increased egocentricity.

Diagnosis

The Hare Psychopathy Checklist-Revised (PCL-R), Psychopathy Checklist: Screening Version (PCL:SV), the P-Scan, the Psychopathy Checklist: Youth Version (PCL:YV), and the Antisocial Process Screening Device (APSD were developed by Dr. Hare as standardized tests to assist and diagnose patients considered with psychopathic tendencies. [20] A ‘normal’ person would obtain a score of 5/40 on this test, whereas the average score for a psychopath would be around 30.

Psychopathy vs ASPD

Psychopaths are often thought to additionally have antisocial personality disorder, since a clear distinction between the two disorders has not been consented upon. In Drislane et al.’s research he makes clear distinctions between the two disorders. To begin psychopaths demonstrate diminished cortical positioning to sudden noxious stimuli through the reduction in probe P3 (noise probe-elicited P300 response) reactivity in response to abrupt noise bursts happening either between or within picture-viewing intervals. Anti Social personality disorder individuals however do not exhibit these effects.

Results suggest psychopaths have diminished assessment of post-processing of displeasuring noise probes. As well as increased distribution of attentional resources to more absorbing observational focus, exemplified in the decrement in probe P3 throughout the inspection of affective compared to neutral images. This general decrease in probe P3 reaction is accredited to the affective-interpersonal constituent of PCL-R psychopathy. The weakening amplitude of the P3 probe during emotionally charged images in contrast to impartial images demonstrates a cortical attenuation post-processing that is independent to the gradation of awareness applied to the perception of the stimuli.

Psychopaths display inadequate fear due to a lack of fear-potentiated shock, whereas ASPD individuals display normal initiation of shock throughout displeasuring prompts. The weakening in P3 relative to affective-interpersonal characteristics of psychopathy can be juxtaposed with weakening of objective stimulus P3 in regular cognitive tasks seen in ASPD individuals. Results imply that insufficient impulse control seen in psychopaths additionally occurs in ASPD. Although psychopathy is explicitly represents the brain’s compromised reactivity to the defensive motivational system.
[8]

Theories

Newman's Theory

Psychopaths exhibit a diminished aptitude to process the significance of contextual environmental cues when involved in goal-directed behavior. They lack a response modulator; that would allow the involuntary shift of attention from the leading response to perceive situational cues and alter behavior appropriately. Psychopathy demonstrate meager performance on passive avoidance and response-reversal tasks, which is associated to their inability or reduced ability to alter behavior once a central response is started. [3]

Blair's Theory

Psychopaths show weakened structures for influence representations. The function of the amygdala is to denote emotional components of reward and punishment to allow for learning. The discrepancy seen in psychopathy is in the programming of emotional valence of stimuli. This accounts for inferior fear conditioning and insufficiencies in passive avoidance and response-reversal learning. Focusing on the malfunction between the amygdala and the ventro-medial prefrontal cortex (vmPFC), Blair proposed the integrated emotion system (IES) to model the discrepancies of psychopathic populations in areas of emotional and social complications. Psychopaths are unable to recognize the “social unconditioned stimuli” such as distress cues, and thus cannot form associations due to the dysfunction of their amygdala. This then further cascades into the inability to identify and learn associations between conditioned stimuli; hence, the decreased response to social prompts, which impede empathy development. [3]

Amygdala

Structural Changes

Psychopathy should be regarded as a continuum of personality and behavioral traits. In the results from neuroimaging criminal psychopaths expose decreased amygdala reactivity during fear conditioning, emotional memory tasks, and images of moral infringement [2]. While perceptual processing of both frightening and enraged facial expressions provoked strong bilateral dorsal and ventral amygdala reactivity. The amygdala is known to have decreased volume and structural irregularities. Research has suggested both over and under activation of the amygdala in fear conditioning tasks [3], causing debates in what could be the exact mechanism at play.

Child studies with elevated levels of CU traits have been found to show lower activation of the amygdala, which is concurrent with inferior execution on fear-recognition tasks. Research demonstrates perceptual processing of both frightening and enraged facial expressions provoked strong bilateral dorsal and ventral amygdala reactivity. [2]

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image source:Moul et al. 2012

Functional Deficits

GABA-ergic intercalated neurons reside amid the basolateral amygdala and the central amygdala. These neurons are considered to supply a feed-forward inhibition system from the basolateral amygdala to the central amygdala. Therefore through stimulating the neurons by the basolateral amygdala a decrease in activation is produced at the central amygdala. This consequently eliminates the fear response, leading to ideas that support a mechanism that independently activates both amygdala regions. [3]

Hot Topic

The recent paper by Carre et al. is a hot topic in Psychopathy. This article examines the neural marks of discrete psychopathic traits in a uniquely large-scale sample size. Their research provides a further understanding on the decreased amygdala management of aguish cues seen in psychopathic patients. The interpersonal facet is a distinctive predictor of independent differences in contributory aggression; Carre et al. assume the interpersonal factor is the primary force in association. Through their separate examination of interpersonal and affective factors unexamined before they demonstrate the inability to learn conditioned stimulus-unconditioned stimulus pairings may further impact a dysfunctional violence inhibition mechanism (VIM). Their results challenge current models by demonstrating a general hypo responsiveness of the amygdala. Regions of the amygdala perform different functions with lifestyle positively associated with dorsal amygdala reactivity to infuriated faces demonstrating hyper respoinsiveness, while the interpersonal aspect of psychopathy negatively associated to frightening faces in both the ventral and dorsal amygdala reactivity. [2]

Reward

Reward processing is connected to the ventral striatum (VS) function in psychopathy. The VS, including the nucleus accumbens and ventromedial regions of the caudate and putamen, are engaged in the processing of motivational salience of stimuli, influencing reward anticipation and prediction, as well as the moderating of appetitive behaviors. A particular study stated that discrete differences within a communal sample in impulsive-antisocial psychopathic traits were positively associated with VS reactivity during anticipation of monetary reward. Thus, discrete differences in psychopathic traits may mirror altered reactivity of not only the amygdala to threat, but also the VS to reward. [2]

Fear Response

Deprived fear-recognition and reduced FPS are situation-specific. In psychopathic populations the precise control of attention proves to normalize in both the fear-recognition and FPS deficits of individuals. Extensive lesions of the amygdala have demonstrated restrained fear-potentiated startle response acquisition in primates. The amygdala is required in associative learning as seen in intense amygdala lesions in animals and humans deficiency in forming association and learning predictive properties of a stimulus. However, psychopaths are able to acquire initial associations, implying that specific areas of the amygdala must be fully functioning to permit preliminary formations of associations. [3]

Newman’s evidence [15] supports the hypothesis of a manifestation of a dominant stimulus-response impedes with the distribution of attention to substitute contextual stimuli.Psychopaths display challenges in reallocating attention once initially distributed [4]. He establishes that when the foundation of a leading stimulus-response was decreased, psychopaths responded as well as non psychopaths to fluctuating value of stimuli, discontinuing the exhibition of discrepancies in passive avoidance tasks. [3]

Fear conditioning experiments demonstrate psychopaths with weakened autonomic response to stimuli, which have formerly been associated with painful or startling stimulus and produced a lower fear-potentiated startle response. Fear expression is regarded as a sequential process through the amygdala. Information regarding the significance and salience of stimuli in the environment is linked to activation of the basolateral amygdala; a principal location of association establishment between impartially aversive stimuli (US) and neutral stimuli that predict their incidence (CS). Information is then transferred to the central amygdala which principally converts valence and emotional importance and the social demonstration of fear. [3]

Empathetic pain vs Personal Pain in psychopaths and non-psychopaths
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image source:Heym et al. 2013

[6]

Empathy

The Dark Triad tests variables such as psychopathy, narcissism, and Machiavellianism. Traditionally men are less empathic than women, and this is reflected in men’s higher scores in all variables of the Dark Triad. All Dark Triad traits and subscales are associated with decreased degrees of empathy; statistical significance was reached especially in connections between empathy and primary psychopathy.[5] Adolescents displaying psychotic traits had diminished activation in the striatum, anterior cingulate cortex, and amygdala areas that govern emotional components of empathic pain. The dangerousness of the psychotic traits considered by PCL:YV scores are associated with decreased reactivity of both the amygdala and rostral anterior cingulate cortex in reaction to others’ pain.[6] Psychopaths demonstrate reduced physiological reactivity to interpersonal suffering. A significant correlation was seen in Lishner et al.’s study for anger in both male and female stating increased levels of anger following reading of the need story versus the neutral story. Psychopathy is correlated with the incompetence to understand affective empathy, and evaluate degrees of emotions. These individuals are inclined to habitually feel negative emotions such as sadness, anger and fear, while rarely feeling positive emotions. However, Lishner et al’s study on their forensic inpatient sample showed higher affective empathy, especially after reading about subjects in need.[7] Begging the question does empathy already exist in the psychopath? Could it exist but be limited to the intellectual task of reading a story, but be impaired in the observational task of reading physical facial cues?

Cingulate Cortex

The cingulate cortex has preliminary roles in depression and schizophrenia; howerver, additionally it has been hypothesized that dysfunction in the ACC can give rise to psychopathy. Adult psychopathic individuals have expressed diminished activity in the anterior cingulate cortex in emotional memory and fear conditioning tasks. Deficits in reinforcement signaling of the ventromedial prefrontal cortex encompass the rostral anterior cingulate cortex, advocating for the impaired affective processing in psychopaths in the rostral anterior cingulate cortex. However, conservation of the dorsal anterior cingulate cortex in negotiating response conflict is suggested. [6]

Prefrontal Cortex

It is alleged by clinicians that individuals with sever expression of psychopathic traits have the skill of planning and premeditation of exploits of self-interest. Dolan’s experiment used individuals with ASPD as well as gradations of psychopathy. A 1996 study by Dias et al.[12] testified in marmoset monkeys a twofold separation between behavioural effects of the dorsal lateral prefrontal cortex and orbitofrontal cortex lesions with that of the lateral prefrontal cortex. He found the lateral PFC to influence attentional set-shifting ability (EDS); which showed insufficiency, while the OFC lesions influences reversal of stimulus-reward relations. In theory the OFC-facilitated response reversal discrepancy is correlated to psychopathy, but further trials are needed to establish stronger acceptance. [11]

Ventromedial Prefrontal Cortex: Functional Deficits

Psychopathy has been associated through fMRI studies to be an anomalous instigation of the amygdala and vmPFC. But further research in resting-fMRI has presented deviant functional connectivity between the vmPFC and amygdala. It is proposed that the vmPFC–amygdala’s communication controls emotion and social behavior. Psychopaths show deficits in decision-making due to impaired incorporation of affective information. It is implied that the amygdala mediates the emotional importance of environmental stimuli, whereas the anterior vmPFC distinguishes the comparative value of possibilities and conclusions during decision making. The integration of DTI and rest-fMRI advocate for a socio-affective impairment indicated in psychopathy might imitate deficits in the interaction between vmPFC and amygdala. Studies on apathetic adolescents exposed diminished functional connectivity amid the amygdala and vmPFC during facial affect processing. [9]

Genetics

MAOA gene

MAOA is a mitochondrial sex linked enzyme that is accountable for breakdown of neurotransmitters such as dopamine, norepinephrine and serotonin. Gene expression of the MAOA gene is disturbed by the polymorphism u-VNTR in the promoter region, with productivity determined by the quantity of tandem repeats. Genetic variation in MAOA impacts susceptibility, environmental effects such as physical abuse can manifest biologically during early development. High MAOA functionality reduces risk for antisocial behavior that is accompanied with mistreatment. In Cicchetti’s study individuals with low MAOA functionality showed greater social behavior compared to individuals with high functionality. However, maltreated children in the low MAOA functionality genotypes revealed increased self-accounted antisocial symptoms. [10]

Oxytocin

Oxytocin has a function in the inhibition of the central amygdala, a study conducted in 2005 demonstrated that the medial central amygdala (CeM) can be impeded from the projections of oxytocin neurons from the lateral central amygdala. Kirsch et al. (2005)[13] observed that oxytocin nasally dispensed decreased amygdala activation during the task of observing faces. Administration of oxytocin didn’t influence individuals who were engaged in the frightening faces recognition tasks, confirming affective recognition endures even with the simultaneous decrease in amygdala activity. A 2009 study [14] additionally illustrated oxytocin’s ability to lengthen the period of gaze at livid faces in the course of affective recognition tasks. It is hypothesized that the distribution of valence to stimuli is a fundamental function of oxytocin in the central amygdala. These findings correspond to Newman’s results [15] exposing psychopaths’ grander fear potentiated startle during distribution of attentiveness to socially relevant stimuli, showing low prosocial behavior due to low oxytocin levels, and a higher functioning central amygdala. [3]

Serotonin

Serotonin might play a critical role in psychopathy. Studies establish that greater expression of the serotonin transporter gene (5-HTT: a gene that encrypts for a protein that detaches serotonin from the synaptic cleft) demonstrate lower amygdala activation during affective facial expressions in those such as psychopaths, in contrast to those with lower manifestation of the gene. Through acute serotonin selective reuptake inhibitor (SSRI) administration and the incorporation of the serotonin precursor tryptophan, detection of pleasure and fright were enhanced. Recognition of frightening appearances is associated with synchronizing observational eye movement to socially appropriate prompts in the basolateral amygdala. Intra-basolateral amygdala injections of SSRI demonstrate growth in contextual conditioned fear response, although not in unconditioned fear. Implying that 5-HT is only included in the conditioned fear mechanism, and higher serotonin levels in the basolateral amygdala is vital for autonomic and emotional fear responses. [3]

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