Posts

What is the Trevor Project?

Published on by Andrew MarshallLeave a comment

Introduction

The Trevor Project is an American non-profit organisation founded in 1998 focused on suicide prevention efforts among lesbian, gay, bisexual, transgender, queer, and questioning (LGBTQ) youth.

Through a toll-free telephone number, it operates The Trevor Lifeline, a confidential service that offers trained counsellors. The stated goals of the project are to provide crisis intervention and suicide prevention services for the aforementioned youths (defined by the organisation as people under 25), as well as to offer guidance and resources to parents and educators in order to foster safe, accepting, and inclusive environments for all youth, at home and at school.

Brief History

The project was founded in 1998 in West Hollywood, California, by Celeste Lecesne, Peggy Rajski, and Randy Stone. They are the creators of the 1994 Academy Award-winning short film Trevor, a dramedy about Trevor, a gay thirteen-year-old boy who, when rejected by friends because of his sexuality, makes an attempt to take his life. When the film was scheduled to air on HBO television in 1998, the filmmakers realised that some of the programme’s young viewers might be facing the same kind of crisis as Trevor, and began to search for a support line to be broadcast during the airing. They discovered that no such helpline existed, and decided to dedicate themselves to forming the resource: an organisation to promote acceptance of LGBTQ youth, and to aid in crisis and suicide prevention among that group.

The Trevor Lifeline was established with seed funds provided by The Colin Higgins Foundation and HBO’s license fee. As a result, it became the first nationwide, around-the-clock crisis and suicide prevention helpline for LGBTQ youth. The project also provides online support to young people through the project’s website, as well as guidance and resources to educators and parents.

In November 2009, the project was contracted by the Tulare County Suicide Prevention Task Force, located in Tulare County, California. With this agreement, the project received public funds for the first time. In June 2009, seven Tulare County volunteers completed The Trevor Project Lifeguard Workshop Facilitator training. Lifeguard workshops have been done in schools in Tulare County municipalities, including Dinuba, Lindsay, Porterville and Visalia, as well as in Hanford in adjacent Kings County.

The Trevor Project has been supported by various celebrities, including Melanie Martinez, Ellen DeGeneres, Troye Sivan, Kathy Griffin, Shay Mitchell, Daniel Radcliffe, Neil Patrick Harris, James Marsden, Chris Colfer, Kim Kardashian, Darren Criss, Dianna Agron, George Takei, Anderson Cooper, John Oliver and Tyler Oakley. In 2021, the first openly gay active NFL player, Carl Nassib used his coming out to also announce a $100,000 donation to The Trevor Project.

Projects

The Trevor Lifeline

The Trevor Lifeline is the only nationwide, around-the-clock crisis and suicide prevention helpline for LGBTQ youth in the United States. The lifeline is a free and confidential service from counsellors trained to listen without judging, and can refer callers to supportive local organisations and groups; this information is also available on the project’s website. The number for the line in the United States is 1-866-488-7386.

TrevorText

TrevorText is a confidential text messaging service provided by The Trevor Project 24 hours a day 7 days a week.

TrevorChat

TrevorChat is a free, confidential, live and secure online messaging service provided by The Trevor Project 24 hours a day 7 days a week.

TrevorSpace

TrevorSpace is an online social networking community for LGBTQ+ youth ages 13 through 24, along with their friends and allies. Youth can create personal profiles, which are verified by the administrators before they are allowed to interact with other profiles, and connect with other young people internationally, as well as find resources within their communities. TrevorSpace is commonly used to receive or give advice and make friends who have shared similar experiences as the user. TrevorSpace is carefully monitored by administrators designated by the project to ensure all content is age-appropriate, youth-friendly and factual. Members over the age of 18 cannot privately message members under the age of 18. TrevorSpace links members to The Trevor Project’s home page, where information about The Trevor Lifeline, “Dear Trevor,” and other resources are available. The software used to create TrevorSpace was donated to the project by Tim Gill, an American software entrepreneur and philanthropist.

Palette Fund Internship Programme

Through the Palette Fund Internship Programme, the project provides for five internships in both its Los Angeles and New York City offices. Interns are placed among the programme, communication, and development departments. The programme provides an opportunity for young people to learn about working in the non-profit sector. Palette Fund internships are specifically designed to introduce young leaders to the LGBTQ movement.

Youth Advisory Council

The Youth Advisory Council serves as a liaison between youth nationwide and the project on issues surrounding suicide, sexuality and gender identity. The council submits recommendations to the project in an effort to increase project visibility and best serve the LGBTQ youth population.

School Workshops

The project’s Lifeguard Workshop Programme uses a structured, age-appropriate curriculum to address topics around sexuality, gender identity, the impacts of language and behaviour, and what it means for young people to feel different. The programme also teaches young people to recognise depression and suicide amongst their peers, the impacts of language and behaviour on LGBTQ youth, and suicide prevention skills in schools.

Fundraisers and Annual Awards Ceremonies

Tyler Oakley’s Fundraiser

On 10 February 2014, YouTube personality Tyler Oakley started a fundraiser to collect $150,000 for the Trevor Project. Oakley set the deadline for the money to be collected by the time of his birthday, 22 March, but the goal was reached after only six days. Oakley later extended the fundraiser and more than $462,000 had been raised as of 29 March. On 31 March the fundraiser ended, with a total of $525,754 raised.

Annual Award Ceremony Fundraisers

The Trevor Project uses annual events to honour individuals and businesses that have been leaders in supporting LGBT rights and advocated against bullying and hate crimes. In 1998, it held the first Cracked Xmas fundraiser in Los Angeles, changing its name to TrevorLIVE Los Angeles in 2010. In 2001, a New York City-based annual event was added, using entertainers to raise financial resources for the organisation. This NYC-based event has had three names, beginning as “A Very Funny Whatever”, changing to TrevorNY in 2007 and then to TrevorLIVE New York in 2011. In the 2018 financial year (August 2017 to July 2018), these special events raised over $3,030,000.

The New York City event is typically held in June each year, and the Los Angeles event is typically held in late November or early December each year.

A variety of awards have been given over time and not all awards are given each year.

What is Sensory Processing Sensitivity?

Published on by Andrew MarshallLeave a comment

Introduction

Sensory processing sensitivity (SPS) is a temperamental or personality trait involving “an increased sensitivity of the central nervous system and a deeper cognitive processing of physical, social and emotional stimuli”.

The trait is characterised by “a tendency to ‘pause to check’ in novel situations, greater sensitivity to subtle stimuli, and the engagement of deeper cognitive processing strategies for employing coping actions, all of which is driven by heightened emotional reactivity, both positive and negative”.

A human with a particularly high measure of SPS is considered to have “hypersensitivity”, or be a highly sensitive person (HSP). The terms SPS and HSP were coined in the mid-1990s by psychologists Elaine Aron and her husband Arthur Aron, who developed the Highly Sensitive Person Scale (HSPS) questionnaire by which SPS is measured. Other researchers have applied various other terms to denote this responsiveness to stimuli that is seen in humans and other species.

According to the Arons and colleagues, people with high SPS make up about 15-20% of the population. Although some researchers consistently related high SPS to negative outcomes, other researchers have associated it with increased responsiveness to both positive and negative influences. Aron and colleagues state that the high-SPS personality trait is not a disorder.

Origin and Development of the Terms

Elaine Aron’s book The Highly Sensitive Person was published in 1996. In 1997 Elaine and Arthur Aron formally identified sensory processing sensitivity (SPS) as the defining trait of highly sensitive persons (HSPs). The popular terms hypersensitivity (not to be confused with the medical term hypersensitivity) or highly sensitive are popular synonyms for the scientific concept of SPS. By way of definition, Aron and Aron (1997) wrote that sensory processing here refers not to the sense organs themselves, but to what occurs as sensory information is transmitted to or processed in the brain. They assert that the trait is not a disorder but an innate survival strategy that has both advantages and disadvantages.

Elaine Aron’s academic journal articles as well as self-help publications for the lay reader have focused on distinguishing high SPS from socially reticent behaviour and disorders with which high SPS can be confused; overcoming the social unacceptability that can cause low self-esteem; and emphasizing the advantages of high SPS to balance the disadvantages emphasized by others.

In 2015, sociologist Elizabeth Bernstein wrote in The Wall Street Journal that HSPs were “having a moment,” noting that several hundred research studies had been conducted on topics related to HSPs’ high sensitivity. The First International Scientific Conference on High Sensitivity or Sensory Processing Sensitivity was held at the Vrije Universiteit Brussel. By 2015, more than a million copies of The Highly Sensitive Person had been sold.

Earlier Research

Research pre-dating the Arons’ coining of the term “high sensitivity” includes that of German medicine professor Wolfgang Klages, who argued in the 1970s that the phenomenon of sensitive and highly sensitive humans is “biologically anchored” and that the “stimulus threshold of the thalamus” is much lower in these persons. As a result, said Klages, there is a higher permeability for incoming signals from afferent nerve fibres so that they pass “unfiltered” to the cerebral cortex.

The Arons (1997) recognised psychologist Albert Mehrabian’s (1976, 1980, 1991) concept of filtering the “irrelevant”, but wrote that the concept implied that the inability of HSPs’ (Mehrabian’s “low screeners”) to filter out what is irrelevant would imply that what is relevant is determined from the perspective of non-HSPs (“high screeners”).

Attributes, Characteristics and Prevalence

Boterberg et al. (2016) describe high SPS as a “temperamental or personality trait which is present in some individuals and reflects an increased sensitivity of the central nervous system and a deeper cognitive processing of physical, social and emotional stimuli”.

People with high SPS report having a heightened response to stimuli such as pain, caffeine, hunger, and loud noises. According to Boterberg et al., these individuals are “believed to be easily overstimulated by external stimuli because they have a lower perceptual threshold and process stimuli cognitively deeper than most other people.” This deeper processing may result in increased reaction time as more time is spent responding to cues in the environment, and might also contribute to cautious behaviour and low risk-taking.

The HSP Scale, initially (1997) a questionnaire designed to measure SPS on a unidimensional scale, was subsequently decomposed into two, three, or four factors or sub-scales. Most components have been associated with traditionally accepted negative psychological outcomes including high stress levels, being easily overwhelmed, increased rates of depression, anxiety, and sleep problems, as well as symptoms of autism; the diathesis-stress model focused on increased vulnerability to negative influences. However, the differential susceptibility theory (DST) and biological sensitivity to context theory (BSCT) and sensory processing sensitivity (SPS) suggest increased plasticity in terms of responsiveness to both positive and negative influences; and the vantage sensitivity (VS) concept emphasizes increased responsiveness to positive experiences. Researchers such as Smolewska et al. (2006) said positive outcomes were more common in individuals with high aesthetic sensitivity, who tend to experience heightened positive emotions in response to rewarding stimuli and more likely to score high on “openness” on the Big Five factors model.

Research in evolutionary biology provides evidence that the trait of SPS can be observed, under various terms, in over 100 nonhuman species, Aron writing that the SPS trait is meant to encompass what personality psychologists have described under various other names. Conversely, Aron has distinguished SPS from what she considers it is not, explicitly distinguishing high SPS from possibly similar-appearing traits or disorders (such as shyness, sensation-seeking, sensory processing disorder, and autism), and further, that SPS may be a basic variable that may underlie multiple other trait differences (such as introversion versus extraversion). Contrary to common misconception, according to Aron HSPs include both introverts and extroverts, and may be simultaneously high-sensation seeking and cautious.

In humans and other species, responsive and unresponsive individuals coexist and consistently display different levels of responsiveness to environmental stimuli, the different levels of responsiveness having corresponding evolutionary costs and benefits. This observation parallels Aron’s assertion that high SPS is not a disorder, but rather a personality trait with attendant advantages and disadvantages. Accordingly, Aron cautions medical professionals against prescribing psychoactive medications to “cure” the trait, which may or may not coexist with an actual disorder.

By 2015 the trait had been documented at various levels of study, including temperament and behaviour psychology, brain function and neuronal sensitization, and genetics. For example, genetic studies provide evidence that higher levels of SPS are linked to the serotonin transporter 5-HTTLPR short/short genotype, polymorphisms in dopamine neurotransmitter genes,[37] and the ADRA2b norepinephrine-related gene variant.

HSP Scale score patterns in adults were thought to be distributed as a dichotomous categorical variable with a break point between 10% and 35%, with Aron choosing a cut-off of the highest-scoring 20% of individuals to define the HSP category. A 2019 review article stated that findings suggest people fall into three sensitivity groups along a normal distribution sensitivity continuum.

What is the Differential Susceptibility Hypothesis?

Published on by Andrew Marshall2 Comments

Introduction

The differential susceptibility hypothesis proposed by Jay Belsky is another interpretation of psychological findings that are usually discussed according to the diathesis-stress model.

Both models suggest that people’s development and emotional affect are differentially susceptible to experiences or qualities of the environment. Where the Diathesis-stress model suggests a distinct and mostly negativity-sensitive group, Belsky describes a group that is sensitive to negative experiences but also to positive experiences. These models may be complementary, if some individuals are dually or uniquely positivity-sensitive, while other people are uniquely negativity-sensitive.

Differential Susceptibility versus Diathesis-Stress

The idea that individuals vary in their responsivity to negative qualities of the environment is generally framed in diathesis-stress or dual-risk terms. That is, some individuals, due to their biological, temperamental and/or behavioural characteristics (i.e. “diathesis” or “risk 1”), are more vulnerable to the adverse effects of negative experiences (i.e., “stress” or “risk 2”), whereas others are relatively resilient with respect to them (see Figure 1, an adaptation of Bakermans-Kranenburg and van IJzendoorn’s (2007) Figure 1). A fundamentally different, even if not competing view, of the very same phenomenon is central to Belsky’s differential susceptibility hypothesis and Boyce and Ellis’ (2005) related notion of biological sensitivity to context: Individuals do not simply vary in the degree to which they are vulnerable to the negative effects of adverse experience but, more generally, in their developmental plasticity.

On this hypothesis, more “plastic” or malleable individuals are more susceptible than others to environmental influences in a for-better-and-for-worse manner. That is, susceptible to both the adverse developmental sequelae associated with negative environments and the positive developmental consequences of supportive ones. Less susceptible individuals, in contrast, are less affected by rearing conditions, be they presumptively supportive or undermining of well being (see Figure 2, an adaptation of Bakermans-Kranenburg and Van IJzendoorn’s (2007) Figure 1).

Figure 1. The diathesis-stress/dual-risk model. Developmental outcome as it relates to environmental quality. A “vulnerable” group experiences negative outcome when exposed to a negative environment, although this group is identical to the other, “resilient” group in a positive environment.
Figure 2. The differential susceptibility model. The lines depict two categorical groups that differ in their responsiveness to the environment: the “plastic” group is disproportionately more affected by both negative and positive environments compared to the “fixed” group.

Theoretical Background

Belsky suggests that evolution might select for some children who are more plastic, and others who are more fixed in the face of, for example, parenting styles.

Belsky offers that ancestral parents, just like parents today, could not have known (consciously or unconsciously) which childrearing practices would prove most successful in promoting the reproductive fitness of offspring – and thus their own inclusive fitness. As a result, and as a fitness optimising strategy involving bet hedging, natural selection might have shaped parents to bear children varying in plasticity. This way, if an effect of parenting had proven counterproductive in fitness terms, those children not affected by parenting would not have incurred the cost of developing in ways that ultimately proved “misguided”.

Importantly, natural selection might favour genetic lines with both plastic and fixed developmental and affective patterns. In other words, there is value to having both kinds at once. In light of inclusive-fitness considerations, children who were less malleable (and more fixed) would have “resistance” to parental influence. This could be adaptable some times, and maladaptive other times. Their fixedness would not only have benefited themselves directly, but even their more malleable siblings indirectly. This is because siblings, like parents and children, have 50% of their genes in common. By the same token, had parenting influenced children in ways that enhanced fitness, then not only would more plastic offspring have benefited directly by following parental leads, but so, too, would their parents and even their less malleable siblings who did not benefit from the parenting they received, again for inclusive-fitness reasons. The overall effect may be to temper some of the variability in parenting. That is, to make more conservative bets.

This line of evolutionary argument leads to the prediction that children should vary in their susceptibility to parental rearing and perhaps to environmental influences more generally. As it turns out, a long line of developmental inquiry, informed by a “transactional” perspective, has more or less been based on this unstated assumption.

Criteria for the Testing of Differential Susceptibility

Belsky, Bakermans-Kranenburg, & Van IJzendoorn, (2007) delineated a series of empirical requirements – or steps – for evidencing the differential susceptibility hypothesis. Particularly they identify tests that distinguish differential susceptibility from other interaction effects including diathesis-stress/dual-risk.

While diathesis-stress/dual-risk arises when the most vulnerable are disproportionately affected in an adverse manner by a negative environment but do not also benefit disproportionately from positive environmental conditions, differential susceptibility is characterised by a cross-over interaction: the susceptible individuals are disproportionately affected by both negative and positive experiences. A further criterion that needs to be fulfilled to distinguish differential susceptibility from diathesis-stress/dual-risk is the independence of the outcome measure from the susceptibility factor: if the susceptibility factor and the outcome are related, diathesis-stress/dual-risk is suggested rather than differential susceptibility. Further, environment and susceptibility factor must also be unrelated to exclude the alternative explanation that susceptibility merely represents a function of the environment. The specificity of the differential-susceptibility effect is demonstrated if the model is not replicated when other susceptibility factors (i.e. moderators) and outcomes are used. Finally, the slope for the susceptible subgroup should be significantly different from zero and at the same time significantly steeper than the slope for the non- (or less-) susceptible subgroup.

Susceptibility Markers and Empirical Evidence

Characteristics of individuals that have been shown to moderate environmental effects in a manner consistent with the differential susceptibility hypothesis can be subdivided into three categories:

  • Genetic factors;
  • Endophenotypic factors; and
  • Phenotypic factors.

Bakermans-Kranenburg and Van IJzendoorn (2006) were the first to test the differential susceptibility hypothesis as a function of Genetic Factors regarding the moderating effect of the dopamine receptor D4 7-repeat polymorphism (DRD4-7R) on the association between maternal sensitivity and externalising behaviour problems in 47 families. Children with the DRD4-7R allele and insensitive mothers displayed significantly more externalising behaviours than children with the same allele but with sensitive mothers. Children with the DRD4-7R allele and sensitive mothers had the least externalising behaviours of all whereas maternal sensitivity had no effect on children without the DRD4-7R allele.

Endophenotypic Factors have been examined by Obradovic, Bush, Stamperdahl, Adler and Boyce’s (2010). They investigated associations between childhood adversity and child adjustment in 338 5-year-olds. Children with high cortisol reactivity were rated by teachers as least prosocial when living under adverse conditions, but most prosocial when living under more benign conditions (and in comparison to children scoring low on cortisol reactivity).

Regarding characteristics of the category of Phenotypic Factors, Pluess and Belsky (2009) reported that the effect of child care quality on teacher-rated socioemotional adjustment varied as a function of infant temperament in the case of 761 4.5-year-olds participating in the NICHD Study of Early Child Care and Youth Development (NICHD Early Child Care Research Network, 2005). Children with difficult temperaments as infants manifest the most and least behaviour problems depending on whether they experienced, respectively, poor or good quality care (and in comparison to children with easier temperaments).

Table 1: List of Proposed Susceptibility Factors that emerge across studies, according to Belsky and colleagues.

What is Scopophobia?

Published on by Andrew Marshall1 Comment

Introduction

Scopophobia, scoptophobia, or ophthalmophobia is an anxiety disorder characterised by a morbid fear of being seen in public or stared at by others.

Similar phobias include erythrophobia, the fear of blushing, and an epileptic’s fear of being looked at, which may itself precipitate such an attack. Scopophobia is also commonly associated with schizophrenia and other psychiatric disorders. Often scopophobia will result in symptoms common with other anxiety disorders. Scopophobia is unique among phobias in that the fear of being looked at is considered both a social phobia and a specific phobia.

Refer to Scopophilia.

Origin of the Term

The term scopophobia comes from the Greek σκοπέω skopeō, “look to, examine”, and φόβος phobos, “fear”. Ophthalmophobia comes from the Greek ὀφθαλμός ophthalmos, “eye”.

Brief History

Phobias have a long history. The concept of social phobias was referred to as long ago as 400 B.C. One of the first references to scopophobia was by Hippocrates who commented on an overly-shy individual, explaining that such a person “loves darkness as light” and “thinks every man observes him.”

The term “social phobia” (phobie sociale) was first coined in 1903 by French psychiatrist Pierre Janet. He used this term to describe patients of his who exhibited a fear of being observed as they were participating in daily activities such as talking, playing the piano or writing.

In 1906 the psychiatric journal The Alienist and Neurologist, described scopophobia:

Then, there is a fear of being seen and a shamefacedness, which one sees in asylums. […] We called it scopophobia — a morbid dread of being seen. In minor degree, it is morbid shamefacedness, and the patient covers the face with his or her hands. In greater degree, the patient will shun the visitor and escape from his or her sight where this is possible. Scopophobia is more often manifest among women than among men.

Later in the same paper (p.285) scopophobia is defined as “a fear of seeing people or being seen, especially of strange faces”.

Signs and Symptoms

Individuals with scopophobia generally exhibit symptoms in social situations when attention is brought upon them like public speaking. Several other triggers exist to cause social anxiety. Some examples include: Being introduced to new people, being teased and/or criticised, embarrassing easily, and even answering a cell phone call in public.

Often scopophobia will result in symptoms common with other anxiety disorders. The symptoms of scopophobia include an irrational feelings of panic, feelings of terror, feelings of dread, rapid heartbeat, shortness of breath, nausea, dry mouth, trembling, anxiety and avoidance. Other symptoms related to scopophobia may be hyperventilation, muscle tension, dizziness, uncontrollable shaking or trembling, excessive eye watering and redness of the eyes.

Related Syndromes

Though scopophobia is a solitary disorder, many individuals with scopophobia also commonly experience other anxiety disorders. Scopophobia has been related to many other irrational fears and phobias. Specific phobias and syndromes that are similar to scopophobia include erythrophobia, the fear of blushing (which is found especially in young people), and an epileptic’s fear of being looked at, which may itself precipitate such an attack. Scopophobia is also commonly associated with schizophrenia and other psychiatric disorders. It is not considered indicative of other disorders, but is rather considered as a psychological problem that may be treated independently.

Sociologist Erving Goffman suggested that shying away from casual glances in the street remained one of the characteristic symptoms of psychosis in public. Many scopophobia patients develop habits of voyeurism or exhibitionism. Another related, yet very different syndrome, scopophilia, is the excessive enjoyment of looking at erotic items.

Causes

Scopophobia is unique among phobias in that the fear of being looked at is considered both a social phobia and a specific phobia, because it is a specific occurrence which takes place in a social setting. Most phobias typically fall in either one category or the other but scopophobia can be placed in both. On the other hand, as with most phobias, scopophobia generally arises from a traumatic event in the person’s life. With scopophobia, it is likely that the person was subjected to public ridicule as a child. Additionally, a person with scopophobia may often be the subject to public staring, possibly due to a physical disability.

According to the Social Phobia/Social Anxiety Association, US government data for 2012 suggests that social anxiety affects over 7% of the population at any given time. Stretched over a lifetime, the percentage increases to 13%.

Psychoanalytic Views

Building on Freud’s concept of the eye as an erogenous zone, psychoanalysts have linked scopophobia to a (repressed) fear of looking, as well as to an inhibition of exhibitionism. Freud also referred to scopophobia as a “dread of the evil eye” and “the function of observing and criticizing the self” during his research into the “eye” and “transformed I’s.”

In some explanations, the equation of being looked at with a feeling of being criticized or despised reveals shame as a motivating force behind scopophobia. In the self-consciousness of adolescence, with its increasing awareness of the Other as constitutive of the looking glass self, shame may exacerbate feelings of erythrophobia and scopophobia.

Treatment

There are several options for treatment of scopophobia. With one option, desensitisation, the patient is stared at for a prolonged period and then describes their feelings. The hope is that the individual will either be desensitised to being stared at or will discover the root of their scopophobia.

Exposure therapy, another treatment commonly prescribed, has five steps:

  • Evaluation.
  • Feedback.
  • Developing a fear hierarchy.
  • Exposure.
  • Building.

In the evaluation stage, the scopophobic individual would describe their fear to the therapist and try to find out when and why this fear developed. The feedback stage is when the therapist offers a way of treating the phobia. A fear hierarchy is then developed, where the individual creates a list of scenarios involving their fear, with each one becoming worse and worse. Exposure involves the individual being exposed to the scenarios and situations in their fear hierarchy. Finally, building is when the patient, comfortable with one step, moves on to the next.

As with many human health problems support groups exist for scopophobic individuals. Being around other people who face the same issues can often create a more comfortable environment.

Other suggested treatments for scopophobia include hypnotherapy, neuro-linguistic programming (NLP), and energy psychology. In extreme cases of scopophobia, it is possible for the subject to be prescribed anti-anxiety medications. Medications may include benzodiazepines, antidepressants, or beta-blockers.

In Popular Culture

  • In The Neverending Story, the Acharis are a race of beings so ashamed of their ugliness that they never appear in daylight.
  • The character Ryōshi Morino in Ōkami-san has the condition, wearing his hair long to avoid eye contact, and breaking down crying when he notices people staring at him.
  • The character Marimo Kaburagi in the second season of the anime series Active Raid has scopophobia, but her symptoms are alleviated by her wearing special glasses which digitally censor the eyes of whomever she looks at.
  • The SCP Foundation character SCP-096 is a humanoid monster that reacts violently whenever its face is seen through any medium, hunting down whoever saw it; this is typically avoided via showing an artistic depiction to prevent direct viewing.

Reference

“The Alienist and Neurologist”, edited by Charles Hamilton Hughes, 1906, p.165, p.285 (digitised by Google).

What is Scopophilia?

Published on by Andrew Marshall1 Comment

Introduction

In psychology and psychiatry, scopophilia or scoptophilia (Ancient Greek: σκοπέω skopeō, “look to”, “to examine” + φῐλῐ́ᾱ philíā, “the tendency towards”) is an aesthetic pleasure drawn from looking at an object or a person.

In human sexuality, the term scoptophilia describes the sexual pleasure that a person derives from looking at prurient objects of eroticism, such as pornography, the nude body, and fetishes, as a substitute for actual participation in a sexual relationship.

Refer to Scopophobia.

Psychoanalysis

Sigmund Freud used the term scopophilia to describe, analyse, and explain the concept of Schaulust, the pleasure in looking, a curiosity which he considered a partial-instinct innate to the childhood process of forming a personality; and that such a pleasure-instinct might be sublimated, either into Aesthetics, looking at objets d’art or sublimated into an obsessional neurosis “a burning and tormenting curiosity to see the female body”, which afflicted the Rat Man patient of the psychoanalyst Freud. From that initial interpretation of Schaulust arose the psycho-medical belief that the inhibition of the scopic drive might lead to actual, physical illness, such as physiologic disturbances of vision and eyesight. In contrast to Freud’s interpretation of the scopic drive, other psychoanalytic theories proposed that the practices of scopophilia might lead to madness – either insanity or a mental disorder – which is the scopophilic person’s retreat from the concrete world of reality into an abstract world of fantasy.

The theoretic bases of scopophilia were developed by the psychoanalyst Otto Fenichel, in special reference to the process and stages of psychological identification. That in developing a personal identity, “a child, who is looking for libidinous purposes … wants to look at an object in order [for it] to ‘feel along with him’.” That the impersonal interaction of scopophilia (between the looker and the looked-at) sometimes replaced personal interactions in the psychological life of a person who is socially anxious, and seeks to avoid feelings of guilt.

Lacan’s conceptual development of the gaze linked the pleasure of scopophilia to the person’s apprehension of the Other (person) who is not the Self; that is: “The gaze is this object lost, and suddenly re-found, in the conflagration of shame, by the introduction of the Other.” The practice of scopophilia is how a person’s desire is captured by the imaginary representation of the Other. Theories alternative to Lacan’s interpretations of scopophilia and the gaze proposed that a child’s discovery of genital difference, and the accompanying anxiety about not knowing the difference of the Other sex, is the experience that subsequently impels the child’s scopic drive to fulfil the desire to look and to look at.

Literary Examples

  • The Satyricon (The Book of Satyr-like Adventures, AD 1st c.), by Gaius Petronius Arbiter, presents the scopophilic description of a priestess of Priapus as the woman who was “the first to put an inquisitive eye to a crack she had naughtily opened, and spy on their play with prurient eagerness.”
  • Secret Sexualities: A Sourcebook of 17th and 18th Century Writing (2003), by Ian McCormick, shows that transgressive sexuality is composed of the inter-relationships between the public and the private spheres and between the open and the secret aspects of a person’s life.
    • The example is Memoirs of a Woman of Pleasure (1749), in which the protagonist Fanny Hill gives her scoptophilic observations of two sodomites, which include descriptions of the furnishings and the décor of the room in which they are copulating: ” .. . at length I observed a paper patch of the same colour as the wainscot, which I took to conceal some flaw; but then it was so high that I was obliged to stand upon a chair to reach it, which I did, as soft as possible, and, with a point of a bodkin, soon pierced it, and opened myself espial room sufficient. And now, applying my eye close, I commanded the room perfectly, and could see my two young sparks romping and pulling one another about, entirely, to my imagination, in frolic and innocent play.”

Race

Critical race theorists, such as bell hooks, in “Eating Each Other” (2006),[15] Shannon Winnubst in “Is the Mirror Racist?: Interrogating the Space of Whiteness” (2006), and David Marriott in “Bordering On: The Black Penis” (1996), present and describe scopophilia and the scopic drive as the psychological and social mechanisms that realise the practices of Other-ing a person to exclude them from society. (c.f. scopophobia) That the social practice of scopophilia is meant to definitively fix the appearance and the identity of the Other (person) who is not the Self, by way of the gaze that objectifies and dehumanises a person as “not I” and thus “not one of us.” In that philosophic vein, the practices of cultural scopophilia restrict the number and type of visible representations of “outsiders” people in a society.

Cinema

In Psycho (1960), directed by Alfred Hitchcock, the protagonist Norman Bates is a voyeur whose motel rooms feature peepholes. In the course of the story, the motel manager Norman spies upon the anti-heroine as she undresses in her ostensibly private room. In Peeping Tom (1960), directed by Michael Powell, Scopophilia is mentioned as a psychological affliction of the protagonist, Mark Lewis. As narrative cinema, Peeping Tom is a deliberate exercise in voyeurism for the protagonist and for the spectator, which demonstrates how readily the protagonist and the spectator are mentally willing and morally capable of watching atrocities (torture, mutilation, death) that should not be gazed upon as narrative movies. The mentally ill protagonist acted as he acted consequent to severe mental mistreatment in boyhood, by his film-maker father; the paternal abuse mentally malformed Mark into a reclusive, introverted man comfortable with torturing and killing people.

In the 1970s, parting from Lacan’s propositions, psychoanalysts of the cinema used the term scopophilia to identify and to describe the aesthetic and emotional pleasures (often pathological), and other unconscious mental processes that occur in the minds spectators gazing at a film. Yet voyeurism and the male gaze are psychological practices basic to the spectators’ emotional experience of viewing mainstream, commercial cinema; notably, the male gaze is fully presented, described, and explained, and contrasted with the female gaze, in the essay “Visual Pleasure and Narrative Cinema” (1975), by Laura Mulvey. Subsequent scholars have challenged Mulvey’s influential reading of scopophilia as a “gross reduction of the erotic and the aesthetic to the politics of representation.”

On This Day … 31 October

Published on by Andrew MarshallLeave a comment

People (Births)

  • 1918 – Ian Stevenson, American psychiatrist and academic (d. 2007).

People (Deaths)

  • 1939 – Otto Rank, Austrian psychologist, author, and educator (b. 1884).

Ian Stevenson

Ian Pretyman Stevenson (31 October 1918 to 08 February 2007) was a Canadian-born American psychiatrist.

He worked for the University of Virginia School of Medicine for fifty years, as chair of the department of psychiatry from 1957 to 1967, Carlson Professor of Psychiatry from 1967 to 2001, and Research Professor of Psychiatry from 2002 until his death.

Otto Rank

Otto Rank (né Rosenfeld; 22 April 1884 to 31 October 1939) was an Austrian psychoanalyst, writer, and philosopher.

Born in Vienna, he was one of Sigmund Freud‘s closest colleagues for 20 years, a prolific writer on psychoanalytic themes, editor of the two leading analytic journals of the era, managing director of Freud’s publishing house, and a creative theorist and therapist.

In 1926, Rank left Vienna for Paris and, for the remainder of his life, led a successful career as a lecturer, writer, and therapist in France and the United States.

What is Psychical Inertia?

Published on by Andrew Marshall1 Comment

Introduction

Psychical inertia is a term introduced by Carl Jung to describe the psyche’s resistance to development and change.

He considered it one of the main reason for the neurotic opposing, or shrinking from, his or her age-appropriate tasks in life.

Refer to Repetition Compulsion.

Freudian and Other Developments

Freud argued that such psychic inertia played a part in the lives of the normal, as well as of the neurotic, and saw its origins in fixation between early instincts and their first impressions of significant objects. As late as Civilization and its Discontents (his 1930 book), he considered as a major obstacle to cultural development “the inertia of the libido, its disinclination to give up an old position for a new one”.

Later Jungians have seen psychic inertia as a force of nature reflecting both internal and outer determinants; while others have seen it as a product of social pressures, especially in relation to ageing.

What is Repetition Compulsion?

Published on by Andrew Marshall1 Comment

Introduction

Repetition compulsion is a psychological phenomenon in which a person repeats an event or its circumstances over and over again.

This includes re-enacting the event or putting oneself in situations where the event is likely to happen again. This “re-living” can also take the form of dreams in which memories and feelings of what happened are repeated, and even hallucinated.

Repetition compulsion can also be used to cover the repetition of behaviour or life patterns more broadly: a “key component in Freud’s understanding of mental life, ‘repetition compulsion’ … describes the pattern whereby people endlessly repeat patterns of behaviour which were difficult or distressing in earlier life”.

Refer to Psychical Inertia.

Freud

Sigmund Freud‘s use of the concept of “repetition compulsion” (German: Wiederholungszwang) was first defined in the article of 1914, Erinnern, Wiederholen und Durcharbeiten (“Remembering, Repeating and Working-Through”). Here he noted how “the patient does not remember anything of what he has forgotten and repressed, he acts it out, without, of course, knowing that he is repeating it … For instance, the patient does not say that he remembers that he used to be defiant and critical toward his parents’ authority; instead, he behaves in that way to the doctor”.

He explored the repetition compulsion further in his 1920 essay Beyond the Pleasure Principle, describing four aspects of repetitive behaviour, all of which seemed odd to him from the point of view of the mind’s quest for pleasure/avoidance of unpleasure.

The first was the way “dreams occurring in traumatic neuroses have the characteristic of repeatedly bringing the patient back into the situation of his accident” rather than, for example, “show[ing] the patient pictures from his healthy past”.

The second came from children’s play. Freud reported observing a child throw his favourite toy from his crib, become upset at the loss, then reel the toy back in, only to repeat this action. Freud theorised that the child was attempting to master the sensation of loss “in allowing his mother to go away without protesting”, but asked in puzzlement “How then does his repetition of this distressing experience as a game fit in with the pleasure principle?”.

The third was the way (noted in 1914) that the patient, exploring in therapy a repressed past, “is obliged to repeat the repressed material as a contemporary experience instead of … remembering it as something belonging to the past … the compulsion to repeat the events of his childhood in the transference evidently disregards the pleasure principle in every way”.

The fourth was the so-called “destiny neurosis”, manifested in “the life-histories of men and women … [as] an essential character-trait which remains always the same and which is compelled to find expression in a repetition of the same experience”.

All such activities appeared to Freud to contradict the organism’s search for pleasure, and therefore “to justify the hypothesis of a compulsion to repeat—something that seems more primitive, more elementary, more instinctual than the pleasure principle which it over-rides”: “a daemonic current/trait”, “a daemonic character”, a “daemonic compulsion”, likely alluding to the Latin motto errare humanum est, perseverare autem diabolicum (“to err is human, to persist [in committing such errors] is of the devil”). Following this line of thought, he would come to stress that “an instinct is an urge inherent in organic life to restore an earlier state of things” (an explanation that some scholars have labelled as “metaphysical biology”), so to arrive eventually at his concept of the death drive.

Along the way, however, Freud had in addition considered a variety of more purely psychological explanations for the phenomena of the repetition compulsion which he had observed. Traumatic repetitions could be seen as the result of an attempt to retrospectively “master” the original trauma, a child’s play as an attempt to turn passivity into activity: “At the outset he was in a passive situation … but by repeating it, unpleasurable though it was, as a game, he took on an active part”.

At the same time, the repetition of unpleasant experiences in analysis could be considered “unpleasure for one system [the ego] and simultaneously satisfaction for the other [the id]. In the second edition of 1921, he extended the point, stating explicitly that transference repetitions “are of course the activities of instincts intended to lead to satisfaction; but no lesson has been learnt from the old experience of these activities having led only to unpleasure”.

Five years later, in Inhibition, Symptom and Anxiety, he would quietly revise his earlier definition – “There is no need to be discouraged by these emendations … so long as they enrich rather than invalidate our earlier views” – in his new formula on “the power of the compulsion to repeat—the attraction exerted by the unconscious prototypes upon the repressed instinctual process”.

Later Psychoanalytic Developments

It was in the later, psychological form that the concept of the repetition compulsion passed into the psychoanalytic mainstream. Otto Fenichel in his “second generation” compendium The Psychoanalytic Theory of Neurosis stressed two main kinds of neurotic repetition.

On the one hand, there were “Repetitions of traumatic events for the purpose of achieving a belated mastery … seen first and most clearly in children’s games”, although the “same pattern occurs in the repetitive dreams and symptoms of traumatic neurotics and in many similar little actions of normal persons who … repeat upsetting experiences a number of times before these experiences are mastered”. Such traumatic repetitions could themselves appear in active or passive forms. In a passive form, one chooses his or her most familiar experiences consistently as a means to deal with problems of the past, believing that new experiences will be more painful than their present situation or too new and untested to imagine. In the active, participatory form, a person actively engages in behaviour that mimics an earlier stressor, either deliberately or unconsciously, so that in particular events that are terrifying in childhood become sources of attraction in adulthood. For instance, a person who was spanked as a child may incorporate this into their adult sexual practices; or a victim of sexual abuse may attempt to seduce another person of authority in his or her life (such as their boss or therapist): an attempt at mastery of their feelings and experience, in the sense that they unconsciously want to go through the same situation but that it not result negatively as it did in the past.

On the other hand, there were “Repetitions due to the tendency of the repressed to find an outlet”. Here the drive of the repressed impulse to find gratification brought with it a renewal of the original defence: “the anxiety that first brought about the repression is mobilized again and creates, together with the repetition of the impulse, a repetition of the anti-instinctual measures”. Fenichel considered that “Neurotic repetitions of this kind contain no metaphysical element”, and “even the repetition of the most painful failure of the Oedipus complex in the transference during a psychoanalytic cure is not ‘beyond the pleasure principle'”.

Later writers would take very similar views. Eric Berne saw as central to his work “the repetition compulsion which drives men to their doom, the power of death, according to Freud … [who] places it in some mysterious biological sphere, when after all it is only the voice of seduction” – the seduction of the repressed and unconscious id.

Erik Erikson saw the destiny neurosis – the way “that some people make the same mistakes over and over” – in the same light: “the individual unconsciously arranges for variations of an original theme which he has not learned either to overcome or to live with”. Ego psychology would subsequently take for granted “how rigidly determined our lives are—how predictable and repetitive … the same mistake over and over again”.

Object relations theory, stressing the way “the transference is a live relationship … in the here-and-now of the analysis, repeating the way that the patient has used his objects from early in life” considered that “this newer conception reveals a purpose … [in] the repetition compulsion”: thus “unconscious hope may be found in repetition compulsion, when unresolved conflicts continue to generate attempts at solutions which do not really work … [until] a genuine solution is found”.

Later Formulations

By the close of the twentieth century, the psychoanalytic view of repetition compulsion had come into increasing dialogue with a variety of other discourses, ranging from attachment theory through brief psychodynamic therapy to cognitive behavioural therapy.

Attachment theory saw early developmental experiences leading to “schemas or mental representations of relationship … [which] become organized, encoded experiential and cognitive data … that led to self-confirmation”.

The core conflictual relationship theme – “core wishes that the individual has in relation to others” – was seen in brief psychodynamic therapy as linked to the way in “a repetition compulsion, the client will behave in ways that engender particular responses from others that conform with previous experiences in interpersonal relationships”.

Psychological schemas – described in cognitive psychology, social psychology, and schema therapy – are “an enduring symbolic framework that organises constellations of thought, feeling, memory, and expectation about self and others”. In some cases psychological schemas may be seen as analogous to the role in psychoanalytic theory of early unconscious fixations in fuelling the repetition compulsion.

What is Perphenazine?

Published on by Andrew Marshall2 Comments

Introduction

Perphenazine is a typical antipsychotic drug. Chemically, it is classified as a piperazinyl phenothiazine. Originally marketed in the United States as Trilafon, it has been in clinical use for decades.

Perphenazine is roughly ten times as potent as chlorpromazine at the dopamine-2 (D2) receptor; thus perphenazine is considered a medium-potency antipsychotic.

Refer to Perphenazine Enanthate.

Medical Uses

In low doses it is used to treat agitated depression (together with an antidepressant). Fixed combinations of perphenazine and the tricyclic antidepressant amitriptyline in different proportions of weight exist (see Etrafon below). When treating depression, perphenazine is discontinued as fast as the clinical situation allows. Perphenazine has no intrinsic antidepressive activity. Several studies show that the use of perphenazine with fluoxetine (Prozac) in patients with psychotic depression is most promising, although fluoxetine interferes with the metabolism of perphenazine, causing higher plasma levels of perphenazine and a longer half-life. In this combination the strong antiemetic action of perphenazine attenuates fluoxetine-induced nausea and vomiting (emesis), as well as the initial agitation caused by fluoxetine. Both actions can be helpful for many patients.

Perphenazine has been used in low doses as a ‘normal’ or ‘minor’ tranquiliser in patients with a known history of addiction to drugs or alcohol, a practice which is now strongly discouraged.

Perphenazine has sedating and anxiolytic properties, making the drug useful for the treatment of agitated psychotic patients.

A valuable off-label indication is the short-time treatment of hyperemesis gravidarum, in which pregnant women experience violent nausea and vomiting. This problem can become severe enough to endanger the pregnancy. As perphenazine has not been shown to be teratogenic and works very well, it is sometimes given orally in the smallest possible dose.

Effectiveness

Perphenazine is used to treat psychosis (e.g. in people with schizophrenia and the manic phases of bipolar disorder). Perphenazine effectively treats the positive symptoms of schizophrenia, such as hallucinations and delusions, but its effectiveness in treating the negative symptoms of schizophrenia, such as flattened affect and poverty of speech, is unclear. Earlier studies found the typical antipsychotics to be ineffective or poorly effective in the treatment of negative symptoms, but two recent, large-scale studies found no difference between perphenazine and the atypical antipsychotics.

Side Effects

As a member of the phenothiazine type of antipsychotics, perphenazine shares in general all allergic and toxic side-effects of chlorpromazine. A 2015 systematic review of the data on perphenazine conducted by the Cochrane Collaboration concluded that “there were no convincing differences between perphenazine and other antipsychotics” in the incidence of adverse effects. Perphenazine causes early and late extrapyramidal side effects more often than placebo, and at a similar rate to other medium-potency antipsychotics and the atypical antipsychotic risperidone.

When used for its strong antiemetic or antivertignosic effects in cases with associated brain injuries, it may obscure the clinical course and interferes with the diagnosis. High doses of perphenazine can cause temporary dyskinesia. As with other typical antipsychotics, permanent or lasting tardive dyskinesia is a risk.

Discontinuation

The British National Formulary recommends a gradual withdrawal when discontinuing antipsychotics to avoid acute withdrawal syndrome or rapid relapse. Symptoms of withdrawal commonly include nausea, vomiting, and loss of appetite. Other symptoms may include restlessness, increased sweating, and trouble sleeping. Less commonly there may be a feeling of the world spinning, numbness, or muscle pains. Symptoms generally resolve after a short period of time.

There is tentative evidence that discontinuation of antipsychotics can result in psychosis. It may also result in reoccurrence of the condition that is being treated. Rarely tardive dyskinesia can occur when the medication is stopped.

Pharmacology

Pharmacokinetics

Perphenazine has an oral bioavailability of approximately 40% and a half-life of 8 to 12 hours (up to 20 hours), and is usually given in 2 or 3 divided doses each day. It is possible to give two-thirds of the daily dose at bedtime and one-third during breakfast to maximise hypnotic activity during the night and to minimise daytime sedation and hypotension without loss of therapeutic activity.

Formulations

It is sold under the brand names Trilafon (single drug) and Etrafon/Triavil/Triptafen (contains fixed dosages of amitriptyline). A brand name in Europe is Decentan pointing to the fact that perphenazine is approximately 10-times more potent than chlorpromazine. Usual oral forms are tablets (2, 4, 8, 16 mg) and liquid concentrate (4 mg/ml).

The ‘Perphenazine injectable USP’ solution is intended for deep intramuscular (IM) injection, for patients who are not willing to take oral medication or if the patient is unable to swallow. Due to a better bioavailability of the injection, two-thirds of the original oral dose is sufficient. The incidence of hypotension, sedation and extrapyramidal side-effects may be higher compared to oral treatment. IM-injections are appropriate for a few days, but oral treatment should start as soon as possible.

In many countries, depot forms of perphenazine exist (as perphenazine enanthate and perphenazine decanoate). One injection works for 1 to 4 weeks depending on the dose of the depot-injection. Depot-forms of perphenazine should not be used during the initial phase of treatment as the rare neuroleptic malignant syndrome may become more severe and uncontrollable with this form. Extrapyramidal side-effects may be somewhat reduced due to constant plasma-levels during depot-therapy. Also, patient compliance is sure, as many patients do not take their oral medication, particularly if feeling better once improvement in psychosis is achieved.

Interactions

Fluoxetine causes higher plasma levels and a longer elimination half-life of perphenazine, therefore a dose reduction of perphenazine might be necessary.

Perphenazine intensifies the central depressive action of drugs with such activity (tranquilizers, hypnotics, narcotics, antihistaminics, OTC-antiemetics etc.). A dose reduction of perphenazine or the other drug may be necessary.

In general, all neuroleptics may lead to seizures in combination with the opioid tramadol (Ultram).

Perphenazine may increase the insulin needs of diabetic patients. Monitor blood glucose levels of insulin-dependent patients regularly during long-term treatment.

What is Paroxetine?

Published on by Andrew Marshall19 Comments

Introduction

Paroxetine, sold under the brand names Paxil and Seroxat among others, is an antidepressant of the selective serotonin reuptake inhibitor (SSRI) class.

It is used to treat major depressive disorder, obsessive-compulsive disorder, panic disorder, social anxiety disorder, posttraumatic stress disorder (PTSD), generalised anxiety disorder (GAD) and premenstrual dysphoric disorder. It has also been used in the treatment of premature ejaculation and hot flashes due to menopause. It is taken by mouth.

Common side effects include drowsiness, dry mouth, loss of appetite, sweating, trouble sleeping, and sexual dysfunction. Serious side effects may include suicidal thoughts in those under the age of 25, serotonin syndrome, and mania. While the rate of side effects appears similar compared to other SSRIs and SNRIs, antidepressant discontinuation syndromes may occur more often. Use in pregnancy is not recommended, while use during breastfeeding is relatively safe. It is believed to work by blocking the re-uptake of the chemical serotonin by neurons in the brain.

Paroxetine was approved for medical use in the United States in 1992 and initially sold by GlaxoSmithKline. It is on the World Health Organisation’s List of Essential Medicines. It is available as a generic medication. In 2019, it was the 78th most commonly prescribed medication in the United States, with more than 9 million prescriptions. In 2018, it was in the top 10 of most prescribed antidepressants in the United States. In 2012, the United States Department of Justice fined GlaxoSmithKline $3 billion for withholding data, unlawfully promoting use in those under 18, and preparing an article that misleadingly reported the effects of paroxetine in adolescents with depression following its clinical trial study 329.

Medical Uses

Paroxetine is primarily used to treat major depressive disorder (MDD), obsessive-compulsive disorder (OCD), PTSD, social anxiety disorder, and panic disorder. It is also occasionally used for agoraphobia, GAD, premenstrual dysphoric disorder and menopausal hot flashes.

Depression

A variety of meta analyses have been conducted to evaluate the efficacy of paroxetine in depression. They have variously concluded that paroxetine is superior or equivalent to placebo and that it is equivalent or inferior to other antidepressants. Despite this, there was no clear evidence that paroxetine was better or worse compared with other antidepressants at increasing response to treatment at any point in time.

Anxiety Disorders

Paroxetine was the first antidepressant approved in the United States for the treatment of panic disorder. Several studies have concluded that paroxetine is superior to placebo in the treatment of panic disorder.

Paroxetine has demonstrated efficacy for the treatment of social anxiety disorder in adults and children. It is also beneficial for people with co-occurring social anxiety disorder and alcohol use disorder. It appears to be similar to a number of other SSRIs.

Paroxetine is used in the treatment of OCD. Comparative efficacy of paroxetine is equivalent to that of clomipramine and venlafaxine. Paroxetine is also effective for children with OCD.

Paroxetine is approved for treatment of PTSD in the United States, Japan and Europe. In the United States it is approved for short-term use.

Paroxetine is also Food and Drug Administration (FDA)-approved for GAD.

Menopausal Hot Flashes

In 2013, low-dose paroxetine was approved in the US for the treatment of moderate-to-severe vasomotor symptoms such as hot flashes and night sweats associated with menopause. At the low dose used for menopausal hot flashes, side effects are similar to placebo and dose tapering is not required for discontinuation.

Fibromyalgia

Studies have also shown paroxetine “appears to be well-tolerated and improve the overall symptomatology in patients with fibromyalgia” but is less robust in helping with the pain involved.

Adverse Effects

Common side effects include drowsiness, dry mouth, loss of appetite, sweating, trouble sleeping, and sexual dysfunction. Serious side effects may include suicide in those under the age of 25, serotonin syndrome, and mania. While the rate of side effects appears similar compared to other SSRIs and SNRIs, antidepressant discontinuation syndromes may occur more often. Use in pregnancy is not recommended while use during breastfeeding is relatively safe.

Paroxetine shares many of the common adverse effects of SSRIs, including (with the corresponding rates seen in people treated with placebo in parentheses):

  • Nausea 26% (9%).
  • Diarrhoea 12% (8%).
  • Constipation 14% (9%).
  • Dry mouth 18% (12%).
  • Somnolence 23% (9%).
  • Insomnia 13% (6%).
  • Headache 18% (17%).
  • Hypomania 1% (0.3%).
  • Blurred vision 4% (1%).
  • Loss of appetite 6% (2%).
  • Nervousness 5% (3%).
  • Paraesthesia 4% (2%).
  • Dizziness 13% (6%).
  • Asthenia (weakness; 15% (6%)).
  • Tremor 8% (2%).
  • Sweating 11% (2%).
  • Sexual dysfunction (≥10% incidence).

Most of these adverse effects are transient and go away with continued treatment. Central and peripheral 5-HT3 receptor stimulation is believed to result in the gastrointestinal effects observed with SSRI treatment. Compared to other SSRIs, it has a lower incidence of diarrhoea, but a higher incidence of anticholinergic effects (e.g. dry mouth, constipation, blurred vision, etc.), sedation/somnolence/drowsiness, sexual side effects, and weight gain.

Due to reports of adverse withdrawal reactions upon terminating treatment, the Committee for Medicinal Products for Human Use (CHMP) at the European Medicines Agency recommends gradually reducing over several weeks or months if the decision to withdraw is made (Refer to discontinuation syndrome below).

Mania or hypomania may occur in 1% of patients with depression and up to 12% of patients with bipolar disorder. This side effect can occur in individuals with no history of mania but it may be more likely to occur in those with bipolar or with a family history of mania.

Suicide

Like other antidepressants, paroxetine may increase the risk of suicidal thinking and behaviour in people under the age of 25. The FDA conducted a statistical analysis of paroxetine clinical trials in children and adolescents in 2004 and found an increase in suicidality and ideation as compared to placebo, which was observed in trials for both depression and anxiety disorders. In 2015 a paper published in The BMJ that reanalysed the original case notes argued that in Study 329, assessing paroxetine and imipramine against placebo in adolescents with depression, the incidence of suicidal behaviour had been under-reported and the efficacy exaggerated for paroxetine.

Sexual Dysfunction

Sexual dysfunction, including loss of libido, anorgasmia, lack of vaginal lubrication, and erectile dysfunction, is one of the most commonly encountered adverse effects of treatment with paroxetine and other SSRIs. While early clinical trials suggested a relatively low rate of sexual dysfunction, more recent studies in which the investigator actively inquires about sexual problems suggest that the incidence is higher than 70%. Symptoms of sexual dysfunction have been reported to persist after discontinuing SSRIs, although this is thought to be occasional.

Pregnancy

Antidepressant exposure (including paroxetine) is associated with shorter duration of pregnancy (by three days), increased risk of preterm delivery (by 55%), lower birth weight (by 75 g or 2.6 oz), and lower Apgar scores (by <0.4 points). The American College of Obstetricians and Gynaecologists recommends that for pregnant women and women planning to become pregnant, paroxetine “be avoided, if possible”, as it may be associated with increased risk of birth defects.

Babies born to women who used paroxetine during the first trimester have an increased risk of cardiovascular malformations, primarily ventricular and atrial septal defects (VSDs and ASDs). Unless the benefits of paroxetine justify continuing treatment, consideration should be given to stopping or switching to another antidepressant. Paroxetine use during pregnancy is associated with about 1.5-1.7-fold increase in congenital birth defects, in particular, heart defects, cleft lip and palate, clubbed feet or any birth defects.

Antidepressant Discontinuation Syndrome

Refer to Antidepressant Discontinuation Syndrome.

Many psychoactive medications can cause withdrawal symptoms upon discontinuation from administration. Evidence has shown that paroxetine has among the highest incidence rates and severity of withdrawal syndrome of any medication of its class. Common withdrawal symptoms for paroxetine include nausea, dizziness, lightheadedness and vertigo; insomnia, nightmares and vivid dreams; feelings of electricity in the body, as well as rebound depression and anxiety. Liquid formulation of paroxetine is available and allows a very gradual decrease of the dose, which may prevent discontinuation syndrome. Another recommendation is to temporarily switch to fluoxetine, which has a longer half-life and thus decreases the severity of discontinuation syndrome.

In 2002, the FDA published a warning regarding “severe” discontinuation symptoms among those terminating paroxetine treatment, including paraesthesia, nightmares, and dizziness. The FDA also warned of case reports describing agitation, sweating, and nausea. In connection with a Glaxo spokesperson’s statement that withdrawal reactions occur only in 0.2% of patients and are “mild and short-lived”, the International Federation of Pharmaceutical Manufacturers Associations said GSK had breached two of the Federation’s codes of practice.

Paroxetine prescribing information posted at GlaxoSmithKline has been updated related to the occurrence of a discontinuation syndrome, including serious discontinuation symptoms.

Overdose

Acute overdosage is often manifested by emesis, lethargy, ataxia, tachycardia, and seizures. Plasma, serum, or blood concentrations of paroxetine may be measured to monitor therapeutic administration, confirm a diagnosis of poisoning in hospitalized patients or to aid in the medicolegal investigation of fatalities. Plasma paroxetine concentrations are generally in a range of 40-400 μg/L in persons receiving daily therapeutic doses and 200-2,000 μg/L in poisoned patients. Postmortem blood levels have ranged from 1-4 mg/L in acute lethal overdose situations. Along with the other SSRIs, sertraline and fluoxetine, paroxetine is considered a low-risk drug in cases of overdose.

Interactions

Interactions with other drugs acting on the serotonin system or impairing the metabolism of serotonin may increase the risk of serotonin syndrome or neuroleptic malignant syndrome (NMS)-like reaction. Such reactions have been observed with SNRIs and SSRIs alone, but particularly with concurrent use of triptans, MAO inhibitors, antipsychotics, or other dopamine antagonists.

The prescribing information states that paroxetine should “not be used in combination with an MAOI (including linezolid, an antibiotic which is a reversible non-selective MAOI), or within 14 days of discontinuing treatment with an MAOI”, and should not be used in combination with pimozide, thioridazine, tryptophan, or warfarin.

Paroxetine interacts with the following cytochrome P450 enzymes:

  • CYP2D6 for which it is both a substrate and a potent inhibitor.
  • CYP2B6 (strong) inhibitor.
  • CYP3A4 (weak) inhibitor.
  • CYP1A2 (weak) inhibitor.
  • CYP2C9 (weak) inhibitor.
  • CYP2C19 (weak) inhibitor.

Paroxetine has been shown to be an inhibitor of G protein-coupled receptor kinase 2 (GRK2).

Pharmacology

Pharmacodynamics

Paroxetine is the most potent and one of the most specific selective serotonin (5-hydroxytryptamine, 5-HT) reuptake inhibitors (SSRIs). It also binds to the allosteric site of the serotonin transporter, similarly, but less potently, than escitalopram. Paroxetine also inhibits the reuptake of norepinephrine to a lesser extent (<50 nmol/L). Based on evidence from four weeks of administration in rats, the equivalent of 20 mg paroxetine taken once daily occupies approximately 88% of serotonin transporters in the prefrontal cortex.

Pharmacokinetics

Paroxetine is well-absorbed following oral administration. It has an absolute bioavailability of about 50%, with evidence of a saturable first pass effect. When taken orally, it achieves maximum concentration in about 6-10 hours and reaches steady-state in 7-14 days. Paroxetine exhibits significant interindividual variations in volume of distribution and clearance. Less than 2% of an oral dose is excreted in urine unchanged.

Paroxetine is a mechanism-based inhibitor of CYP2D6.

Society and Culture

GlaxoSmithKline has paid substantial fines, paid settlements in class-action lawsuits, and become the subject of several highly critical books about its marketing of paroxetine, in particular the off-label marketing of paroxetine for children, the suppression of negative research results relating to its use in children, and allegations that it failed to warn consumers of substantial withdrawal effects associated with use of the drug. Paroxetine was approved for medical use in the United States in 1992 and initially sold by GlaxoSmithKline. It is currently available as a generic medication. In 2017, it was the 68th most commonly prescribed medication in the United States, with more than eleven million prescriptions. The United States Department of Justice fined GlaxoSmithKline $3 billion in 2012, for withholding data, unlawfully promoting use in those under 18, and preparing an article that misleadingly reported the effects of paroxetine in adolescents with depression following its clinical trial study 329.

Marketing

In early 2004, GSK agreed to settle charges of consumer fraud for $2.5 million. The legal discovery process also uncovered evidence of deliberate, systematic suppression of unfavourable Paxil research results. One of GSK’s internal documents read, “It would be commercially unacceptable to include a statement that efficacy [in children] had not been demonstrated, as this would undermine the profile of paroxetine”.

In 2012 the US Justice Department announced that GSK agreed to plead guilty and pay a $3 billion fine, in part for promoting the use of Paxil for children.

On 12 February 2016, the UK Competition and Markets Authority imposed record fines of £45 million on companies which were found to have infringed European Union and UK Competition law by entering into agreements to delay the market entry of generic versions of the drug in the UK. GlaxoSmithKline received the bulk of the fines, being fined £37,600,757. Other companies, which produce generics, were issued fines which collectively total £7,384,146. UK public health services are likely to claim damages for being overcharged in the period where the generic versions of the drug were illegally blocked from the market, as the generics are over 70% less expensive. GlaxoSmithKline may also face actions from other generics manufacturers who incurred loss as a result of the anticompetitive conduct. On 18 April 2016, appeals were lodged with the Competition Appeal Tribunal by the companies which were fined.

GSK marketed paroxetine through television advertisements throughout the late 1990s and early 2000s. Commercials also aired for the CR version of the drug beginning in 2003.

Sales

In 2007, paroxetine was ranked 94th on the list of bestselling drugs, with over $1 billion in sales. In 2006, paroxetine was the fifth-most prescribed antidepressant in the US retail market, with more than 19.7 million prescriptions. In 2007, sales had dropped slightly to 18.1 million but paroxetine remained the fifth-most prescribed antidepressant in the US.

Trade Names

Trade names include Aropax, Brisdelle, Deroxat, Paxil, Pexeva, Paxtine, Paxetin, Paroxat, Paraxyl, Sereupin, Daparox and Seroxat.

Research

Several studies have suggested that paroxetine can be used in the treatment of premature ejaculation. In particular, intravaginal ejaculation latency time (IELT) was found to increase with 6- to 13-fold, which was somewhat longer than the delay achieved by the treatment with other SSRIs (fluvoxamine, fluoxetine, sertraline, and citalopram). However, paroxetine taken acutely (“on demand”) 3-10 hours before coitus resulted only in a “clinically irrelevant and sexually unsatisfactory” 1.5-fold delay of ejaculation and was inferior to clomipramine, which induced a fourfold delay.

There is also evidence that paroxetine may be effective in the treatment of compulsive gambling and hot flashes.

Benefits of paroxetine prescription for diabetic neuropathy or chronic tension headache are uncertain.

Although the evidence is conflicting, paroxetine may be effective for the treatment of dysthymia, a chronic disorder involving depressive symptoms for most days of the year.

There is evidence to support that paroxetine selectively binds to and inhibits G protein-coupled receptor kinase 2 (GRK2). Since GRK2 regulates the activity of the beta adrenergic receptor, which becomes desensitised in cases of heart failure, paroxetine (or a paroxetine derivative) could be used as a heart failure treatment in the future.

Paroxetine has been deemed to have dmoad activity.