This is a continuation from a previous piece. For the first part of the list, read Part 1.
18. Personality Disorders:
Personality disorders are seen more in people receiving extensive medical and psychiatric services (Samuels, 2011). and while narcissistic personality disorder and Schizotypal personality disorders are relatively rare, borderline, avoidant, and OCPD has been established by meta-analysis to be quite common in both the community and clinical populations (Halter, Pollard, & Jakubec, 2018, P. 434). While studies vary in their estimates of prevalence depending on their methodologies, the ICD-10 suggests that personality disorders affect about 10% of the world’s population (Samuels, 2011). Culture has a definite influence on the rate of diagnosing personality disorders. For example, an Australian study reported substantially higher prevalence rates than North American studies (Samuels, 2011). Differences may reflect the view of personality and behaviour as deviant rather than normal in a particular culture and within certain study methods or it could reflect better-diagnosing practices or a system that has more resources to assist people with personality disorders (Halter, Pollard, & Jakubec, 2018, P. 434).
Personality disorders often co-occur with disorders of mood, eating, anxiety, and substance misuse and they often amplify emotional dysregulation (Halter, Pollard, & Jakubec, 2018, P. 434). Cluster B personality disorder may mute as the individual ages and becomes less impulsive. This dampening may be due to a general tuning down of neurotransmitters (Rosowsky, Abrams, & Zwieg, 2013).
Other disorders such as Obsessive Compulsive Personality Disorder (OCPD) or Paranoid Personality Disorder (PPD) may worsen with age, possibly due to anxiety regarding declining sensory and cognitive capacity (Halter, Pollard, & Jakubec, 2018, P. 434). While genetics are thought to influence the development of personality disorders, individual genes are not believed to be associated with particular personality traits so the relationship among genes and traits is complex (Taylor, Asmundson, & Jane, 2011). The chemical neurotransmitter theory proposes that certain neurotransmitters, including neuron hormones, may regulate and influence temperament (Halter, Pollard, & Jakubec, 2018, P. 434). Research in brain imaging has also revealed some differences in the size and function of specific structures of the brain in people with some personality disorders (Leichsenring, Leibing, Kruse, et al., 2011). Behavioural genetics research has shown that about half of the variance accounting for personality disorders emerges from the environment (Hernandez, Arntz, Gaviria, et al., 2012). Childhood neglect and trauma have been established as risk factors for personality disorders (Samuels, 2011). This association has been linked to possible biological mechanisms involving corticotropin-releasing hormone in response to early life stress and emotional reactivity (Lee, Hempel, Tenharmsel, et al., 2012).
In PTSD, people exposed to trauma undergo “re-experiencing” in the form of recurrent dreams about the traumatic event and unusually vivid and intrusive memories (flashbacks) of the incident. Persistent negative mood and cognitions are common, leading to frequent impairments in daily functioning (APA, 2013). PTSD affects between 3 and 4 percent of American adults in a given year (Kessler et al., 2007), although more than 12 percent of lower Manhattan residents developed the disorder as a consequence of the terrorist attacks of 9/11 (DiGrande et al., 2008). Twice as many women as men develop PTSD. Children appear more vulnerable than adults, with 25 percent of children as opposed to 15 percent of their parents developing PTSD following automobile accidents in which they suffer injuries (de Vries et al., 1999). Combat continues to be one of the most common experiences related to the development of PTSD. Between 8.5 percent and 14 percent of combat soldiers serving in Iraq and Afghanistan experienced severe impairment due to PTSD, and up to 31 percent experienced some impairment (Thomas et al., 2010).
Post-traumatic stress disorder symptoms may start within one month of a traumatic event, but sometimes symptoms may not appear until years after the event (Mayo Clinic, 2018). Early life trauma may result in long term hyperactivity of the Central Nervous System Corticotropin-releasing factor (CRF). The CRF is produced in the hypothalamus, which sends a message to the pituitary gland (located underneath the hypothalamus) which sends a message to the adrenal glands (located above the kidneys) to release the stress hormones Cortisol, Epinephrine, and Norepinephrine. Long term activity of the CRF can have a neurotoxin effect on the hippocampus, which leads to neuron loss (Halter, Pollard, & Jakubec, 2018, P. 251). Research shows that individuals with PTSD have smaller hippocampi, which could explain why individuals with PTSD have trouble with memory (Logue et al., 2018, P. 244-253). Neurotransmitters implicated in PTSD are dopamine, GABA, and norepinephrine (Sherin, 2011, P. 263-278)
Currently, schizophrenia is diagnosed by the presence of symptoms or their precursors for a period of six months (APA, 2013, P. 99) while two or more symptoms, such as hallucinations, delusions, disorganized speech, and grossly disorganized or catatonic behavior, must be significant and last for at least one month (APA, 2013, P. 99). Symptoms of schizophrenia are divided into categories of positive and negative symptoms. Positive symptoms are behaviors that are not expected to occur normally, such as hallucinations and delusions. Instances of these behaviors are frequently referred to as “psychotic episodes:’ Negative symptoms, such as diminished emotional expression and avolition (lack of motivation), occur when normal behaviors are missing (Freberg, 2017, P. 566-567).
A possible etiology for schizophrenia is due to abnormal levels of dopamine. The dopamine hypothesis of schizophrenia suggests that a dysregulated dopamine system contributes to positive, negative, and cognitive symptoms of the disease (Hirvonen & Hietala, 2014).
Hyperactivity of dopamine D2 receptor neurotransmission in subcortical and limbic brain regions contributes to positive symptoms of schizophrenia, whereas negative and cognitive symptoms of the disorder can be attributed to hypofunctionality of dopamine D1 receptor neurotransmission in the prefrontal cortex (Toda & Abi-Dargham, 2007). In support of this, studies have shown an increased density of the dopamine D2 receptor in post-mortem brain tissue of schizophrenia sufferers (Seeman et al., 2000). It is also reported that upregulation of D2 receptors in the caudate nucleus of patients with schizophrenia directly correlates with poorer performance in cognitive tasks involving corticostriatal pathways (Hirvonen et al., 2004). Dopamine-releasing drugs, such as amphetamines, posses psychotomimetic properties (meaning they mimic things like delusions and psychosis) in addition to the D2-antagonist property common to many of the currently prescribed antipsychotic treatments, giving credence to the dopamine hypothesis of schizophrenia (Desbonnet, 2016).
The dopamine hypothesis was first formulated in 1966 when chlorpromazine, a 1st generation (typical) antipsychotic, was found to be an antagonist (blocks or dampens) to dopamine. When this happened, the positive symptoms of schizophrenia were lessened.
A growing body of evidence also suggests that glutamate plays a key role in the etiology of the disease as well. Research so far suggests that insufficient glutamate activity may cause symptoms, partly through its interactions with other neurotransmitters like dopamine and gamma-aminobutyric acid (GABA) (Marsman, et al., 2013, P. 120-129; Howes, McCutcheon, & Stone, 2015, P. 97-115).
The NMDA receptor dysfunction hypothesis of schizophrenia arose initially from the observation that non-competitive NMDA receptor antagonists, including phencyclidine (PCP), dizocilpine, and ketamine, lead to immediate psychological effects, which closely resemble symptoms that occur in schizophrenia, including both positive and negative symptom domains (Javitt, 2007; Krystal et al.,1994; Morgan and Curran, 2006). Psychotic-like symptoms are also seen in chronic ketamine users (Morgan et al., 2009; Stone et al., 2014). Although many glutamate receptors have been implicated, the prevailing hypothesis is for the primary involvement of NMDA receptor dysfunction (Stone et al., 2007).