Tag: Anxiety Disorders

What are Racing Thoughts?

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Introduction

Racing thoughts refers to the rapid thought patterns that often occur in manic, hypomanic, or mixed episodes.

While racing thoughts are most commonly described in people with bipolar disorder and sleep apnoea, they are also common with anxiety disorders, OCD, and other psychiatric disorders such as attention deficit hyperactivity disorder. Racing thoughts are also associated with sleep deprivation, hyperthyroidism and the use of amphetamines.

Description

Racing thoughts may be experienced as background or take over a person’s consciousness. Thoughts, music, and voices might be zooming through one’s mind as they jump tangentially from one to the next. There also might be a repetitive pattern of voice or of pressure without any associated “sound”. It is a very overwhelming and irritating feeling, and can result in losing track of time. In some cases, it may also be frightening to the person experiencing it, as there is a loss of control. If one is experiencing these thoughts at night when going to sleep, they may suddenly awaken, startled and confused by the very random and sudden nature of the thoughts.

Racing thoughts differ in manifestation according to the individual’s perspective. These manifestations can vary from unnoticed or minor distractions to debilitating stress, preventing the sufferer from maintaining a thought.

Generally, racing thoughts are described by an individual who has had an episode where the mind uncontrollably brings up random thoughts and memories and switches between them very quickly. Sometimes they are related, as one thought leads to another; other times they seem completely random. A person suffering from an episode of racing thoughts has no control over their train of thought, and it stops them from focusing on one topic or prevents sleeping.

Associated Conditions

The causes of racing thoughts are most often associated with anxiety disorders, but many influences can cause these rapid, racing thoughts. There are also many associated conditions, in addition to anxiety disorders, which can be classified as having secondary relationships with causing racing thoughts. The conditions most commonly linked to racing thoughts are bipolar disorder, anxiety disorder, attention deficit hyperactivity disorder, sleep deprivation, amphetamine dependence, and hyperthyroidism.

Anxiety Disorders

Racing thoughts associated with anxiety disorders can be caused by many different conditions, such as obsessive-compulsive disorder (OCD), panic disorder, generalised anxiety disorder, or posttraumatic stress disorder.

In people with OCD, racing thoughts can be brought on by stressors, or triggers, causing disturbing thoughts in the individual. These disturbing thoughts, then, result in compulsions characterising OCD in order to lower the stress and gain some sort of control over these stressful, racing thoughts.

Panic disorder is an anxiety disorder characterised by repeated panic attacks of fear or nervousness, lasting several minutes. During these panic attacks, the response is out of proportion to the situation. The racing thoughts may feel catastrophic and intense, but they are a symptom of the panic attack and must be controlled in order to soothe the panic and minimise the panic attack.

Generalised anxiety disorder (GAD) is a neurological anxiety disorder that involves uncontrollable and excessive worrying about irrational topics or problems. These stressful thoughts must be present for at least six months in order to be diagnosed as GAD. Along with other symptoms, racing thoughts is one of the most common ones. With GAD, there is an inability to relax or let thoughts or worries go, persistent worrying and obsessions about small concerns that are out of proportion to the result, and even worrying about their excessive worrying.

Bipolar Disorder

Racing thoughts can be brought on by bipolar disorder, defined by mood instability that range from extreme emotional highs, mania, to severe depression. During the manic phase of bipolar disorder is when racing thoughts usually occur. Disjointed, constantly changing thoughts with no underlying theme can be a sign of the manic phase of bipolar disorder. Manic thoughts can prevent performance of daily routines due to their rapid, unfocused and overwhelming nature. Racing thoughts in people with bipolar disorder are generally accompanied with other symptoms associated with this disorder.

Amphetamines

Amphetamines are used as a stimulant to trigger the central nervous system, increasing heart rate and blood pressure while decreasing appetite. Since amphetamines are a stimulant, use of these drugs result in a state that resembles the manic phase of bipolar disorder and also produces similar symptoms, as stated above.

Attention Deficit Hyperactivity Disorder

Racing thoughts associated with ADHD is most common in adults. With ADHD, racing thoughts can occur and tend to cause insomnia. Racing thoughts in people with ADHD tend to be rapid, unstable thoughts which do not follow any sort of pattern, similar to racing thoughts in people with bipolar disorder. Medications used to treat ADHD, such as Adderall or Methylphenidate, can be prescribed to patients with ADHD to calm these racing thoughts, most commonly in the morning when people wake up but just as well in the evening before sleep.

Lack of Sleep

Racing thoughts, also referred to as “racing mind”, may prevent a person from falling asleep. Chronic sleep apnoea and prolonged disturbed sleep patterns may also induce racing thoughts. Treatment for sleep apnoea and obstructive airway disorder can improve airflow and improve sleep resulting in improved brain and REM (rapid eye movement) function and reduced racing thought patterns.

Hyperthyroidism

Hyperthyroidism is a condition in which the thyroid gland produces too much thyroid hormone, thyroxin. This overabundance of thyroxin causes irregular and rapid heartbeat, irritability, weight loss, nervousness, anxiety and racing thoughts. The anxiety and inability to focus is very common in hyperthyroidism and leads to racing thoughts, as well as panic attacks and difficulty concentrating.

Frequency

Anxiety disorder, the most common mental illness in the United States, affects 40 million people, ages 10 and older; this accounts for 18% of the US population. Most people suffering from anxiety disorder report some form of racing thoughts symptom.

The prevalence of OCD in every culture studied is at least 2% of the population, and the majority of those have obsessions, or racing thoughts. With these reports, estimates of more than 2 million people in the United States (as of 2000) suffer from racing thoughts.

Treatment

There are various treatments available to calm racing thoughts, some of which involve medication. One type of treatment involves writing out the thoughts onto paper. Some treatments suggest using activities, such as painting, cooking, and other hobbies, to keep the mind busy and distract from the racing thoughts. Exercise may be used to tire the person, thereby calming their mind. When racing thoughts are anxiety induced during panic or anxiety attacks, it is recommended that the person wait it out. Using breathing and meditation techniques to calm the breath and mind simultaneously is another tool for handling racing thoughts induced by anxiety attacks. Mindfulness meditation has also shown to help with racing thoughts by allowing practitioners to face their thoughts head-on, without reacting.

While all of these techniques can be useful to cope with racing thoughts, it may prove necessary to seek medical attention and counsel. Since racing thoughts are associated with many other underlying mental illnesses, such as bipolar disorder, anxiety disorder, and ADHD, medications used commonly to treat these disorders will help calm racing thoughts in patients.

Treatment for the underlying causes of racing thoughts is helpful and useful in order to calm the racing thoughts more permanently. For example, in people with ADHD, medications used to promote focus and calm distracting thoughts, will help them with their ADHD.

Some obstructive airway disorders may be relieved with nasal septoplasty which can improve sleep and lead to a reduction of racing mind. Insomnia may increase racing thoughts and those effected will find sleep apnoea treatment and nasal surgery helpful to eliminate their racing thoughts.

It is important to look at the underlying defect that may be causing racing thoughts in order to prevent them in the long-term.

What is Agoraphobia?

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Introduction

Agoraphobia is a mental and behavioural disorder, specifically an anxiety disorder characterised by symptoms of anxiety in situations where the person perceives their environment to be unsafe with no easy way to escape.

These situations can include open spaces, public transit, shopping centres, or simply being outside their home. Being in these situations may result in a panic attack. Those affected will go to great lengths to avoid these situations. In severe cases people may become completely unable to leave their homes.

Agoraphobia is believed to be due to a combination of genetic and environmental factors. The condition often runs in families, and stressful or traumatic events such as the death of a parent or being attacked may be a trigger. In the DSM-5 agoraphobia is classified as a phobia along with specific phobias and social phobia. Other conditions that can produce similar symptoms include separation anxiety, post-traumatic stress disorder, and major depressive disorder. The diagnosis of agoraphobia has been shown to be comorbid with depression, substance abuse, and suicide ideation.

Without treatment it is uncommon for agoraphobia to resolve. Treatment is typically with a type of counselling called cognitive behavioural therapy (CBT). CBT results in resolution for about half of people. In some instances those with a diagnosis of agoraphobia have reported taking benzodiazepines and antipsychotics augmentation. Agoraphobia affects about 1.7% of adults. Women are affected about twice as often as men. The condition often begins in early adulthood and becomes less common in old age. It is rare in children.

Refer to Hikikomori.

Etymology

The term “agoraphobia” was coined in German in 1871 by pioneering German psychologist Carl Friedrich Otto Westphal, 1833-1890, in his article “Die Agoraphobie, eine neuropathische Erscheinung.” Archiv für Psychiatrie und Nervenkrankheiten, Berlin, 1871-1872; 3: 138-161. It is derived from Greek ἀγορά, agorā́, meaning a “place of assembly” or “market-place” and -φοβία, -phobía, meaning “fear”.

Signs and Symptoms

Agoraphobia is a condition where sufferers become anxious in unfamiliar environments or where they perceive that they have little control. Triggers for this anxiety may include wide-open spaces, crowds (social anxiety), or travelling (even short distances). Agoraphobia is often, but not always, compounded by a fear of social embarrassment, as the agoraphobic fears the onset of a panic attack and appearing distraught in public. Most of the time they avoid these areas and stay in the comfort of their haven, usually their home.

Agoraphobia is also defined as “a fear, sometimes terrifying, by those who have experienced one or more panic attacks”. In these cases, the sufferer is fearful of a particular place because they have experienced a panic attack at the same location at a previous time. Fearing the onset of another panic attack, the sufferer is fearful or even avoids a location. Some refuse to leave their homes even in medical emergencies because the fear of being outside of their comfort areas is too great.

The sufferers can sometimes go to great lengths to avoid the locations where they have experienced the onset of a panic attack. Agoraphobia, as described in this manner, is actually a symptom professionals check when making a diagnosis of panic disorder. Other syndromes like obsessive compulsive disorder or post-traumatic stress disorder can also cause agoraphobia. Essentially, any irrational fear that keeps one from going outside can cause the syndrome.

Agoraphobics may suffer from temporary separation anxiety disorder when certain other individuals of the household depart from the residence temporarily, such as a parent or spouse, or when the agoraphobic is left home alone. Such temporary conditions can result in an increase in anxiety or a panic attack or feeling the need to separate themselves from family or maybe friends.

People with agoraphobia sometimes fear waiting outside for long periods of time; that symptom can be called “macrophobia”.

Panic Attacks

Agoraphobia patients can experience sudden panic attacks when traveling to places where they fear they are out of control, help would be difficult to obtain, or they could be embarrassed. During a panic attack, epinephrine is released in large amounts, triggering the body’s natural fight-or-flight response. A panic attack typically has an abrupt onset, building to maximum intensity within 10 to 15 minutes, and rarely lasts longer than 30 minutes. Symptoms of a panic attack include palpitations, rapid heartbeat, sweating, trembling, nausea, vomiting, dizziness, tightness in the throat, and shortness of breath. Many patients report a fear of dying, fear of losing control of emotions, or fear of losing control of behaviours.

Causes

Agoraphobia is believed to be due to a combination of genetic and environmental factors. The condition often runs in families, and stressful or traumatic events such as the death of a parent or being attacked may be a trigger.

Research has uncovered a link between agoraphobia and difficulties with spatial orientation. Individuals without agoraphobia are able to maintain balance by combining information from their vestibular system, their visual system, and their proprioceptive sense. A disproportionate number of agoraphobics have weak vestibular function and consequently rely more on visual or tactile signals. They may become disoriented when visual cues are sparse (as in wide-open spaces) or overwhelming (as in crowds). Likewise, they may be confused by sloping or irregular surfaces.[20] In a virtual reality study, agoraphobics showed impaired processing of changing audiovisual data in comparison with subjects without agoraphobia.

Substance-Induced

Chronic use of tranquilisers and sleeping pills such as benzodiazepines has been linked to onset of agoraphobia. In 10 patients who had developed agoraphobia during benzodiazepine dependence, symptoms abated within the first year of assisted withdrawal. Similarly, alcohol use disorders are associated with panic with or without agoraphobia; this association may be due to the long-term effects of alcohol consumption causing a distortion in brain chemistry. Tobacco smoking has also been associated with the development and emergence of agoraphobia, often with panic disorder; it is uncertain how tobacco smoking results in anxiety-panic with or without agoraphobia symptoms, but the direct effects of nicotine dependence or the effects of tobacco smoke on breathing have been suggested as possible causes. Self-medication or a combination of factors may also explain the association between tobacco smoking and agoraphobia and panic.

Attachment Theory

Some scholars have explained agoraphobia as an attachment deficit, i.e. the temporary loss of the ability to tolerate spatial separations from a secure base. Recent empirical research has also linked attachment and spatial theories of agoraphobia.

Spatial Theory

In the social sciences, a perceived clinical bias exists in agoraphobia research. Branches of the social sciences, especially geography, have increasingly become interested in what may be thought of as a spatial phenomenon. One such approach links the development of agoraphobia with modernity. Factors considered contributing to agoraphobia within modernity are the ubiquity of cars and urbanisation. These have helped develop the expansion of public space and the contraction of private space, thus creating in the minds of agoraphobia-prone people a tense, unbridgeable gulf (a colloquialism) between the two.

Evolutionary Psychology

An evolutionary psychology view is that the more unusual primary agoraphobia without panic attacks may be due to a different mechanism from agoraphobia with panic attacks. Primary agoraphobia without panic attacks may be a specific phobia explained by it once having been evolutionarily advantageous to avoid exposed, large, open spaces without cover or concealment. Agoraphobia with panic attacks may be an avoidance response secondary to the panic attacks, due to fear of the situations in which the panic attacks occurred.

Diagnosis

Most people who present to mental health specialists develop agoraphobia after the onset of panic disorder. Agoraphobia is best understood as an adverse behavioural outcome of repeated panic attacks and subsequent anxiety and preoccupation with these attacks that leads to an avoidance of situations where a panic attack could occur. Early treatment of panic disorder can often prevent agoraphobia. Agoraphobia is typically determined when symptoms are worse than panic disorder, but also do not meet the criteria for other anxiety disorders such as depression. In rare cases where agoraphobics do not meet the criteria used to diagnose panic disorder, the formal diagnosis of agoraphobia without history of panic disorder is used (primary agoraphobia).

Treatments

Therapy

Systematic desensitisation can provide lasting relief to the majority of patients with panic disorder and agoraphobia. The disappearance of residual and sub-clinical agoraphobic avoidance, and not simply of panic attacks, should be the aim of exposure therapy. Many patients can deal with exposure easier if they are in the company of a friend on whom they can rely. Patients must remain in the situation until anxiety has abated because if they leave the situation, the phobic response will not decrease and it may even rise.

A related exposure treatment is in vivo exposure, a cognitive behavioural therapy method, that gradually exposes patients to the feared situations or objects. This treatment was largely effective with an effect size from d = 0.78 to d = 1.34, and these effects were shown to increase over time, proving that the treatment had long-term efficacy (up to 12 months after treatment).

Psychological interventions in combination with pharmaceutical treatments were overall more effective than treatments simply involving either CBT or pharmaceuticals. Further research showed there was no significant effect between using group CBT versus individual CBT.

Cognitive restructuring has also proved useful in treating agoraphobia. This treatment involves coaching a participant through a dianoetic discussion, with the intent of replacing irrational, counterproductive beliefs with more factual and beneficial ones.

Relaxation techniques are often useful skills for the agoraphobic to develop, as they can be used to stop or prevent symptoms of anxiety and panic.

Videoconferencing Psychotherapy (VCP)

Videoconferencing psychotherapy (VCP) is an emerging modality used to treat various disorders in a remote method. Similar to traditional face-to-face interventions, VCP can be used to administer CBT. The use of VCP has been shown to be equally effective as face-to-face interventions at treating panic disorder and agoraphobia (PDA) and motivating the client to continue treatment.

Medications

Antidepressant medications most commonly used to treat anxiety disorders are mainly selective serotonin reuptake inhibitors (SSRIs). Benzodiazepines, monoamine oxidase inhibitor, and tricyclic antidepressants are also sometimes prescribed for treatment of agoraphobia. Antidepressants are important because some have anxiolytic effects. Antidepressants should be used in conjunction with exposure as a form of self-help or with CBT. A combination of medication and CBT is sometimes the most effective treatment for agoraphobia.

Benzodiazepines and other anxiolytic medications such as alprazolam and clonazepam are used to treat anxiety and can also help control the symptoms of a panic attack.

Alternative Medicine

Eye movement desensitisation and reprocessing (EMDR) has been studied as a possible treatment for agoraphobia, with poor results. As such, EMDR is only recommended in cases where cognitive-behavioural approaches have proven ineffective or in cases where agoraphobia has developed following trauma.

Many people with anxiety disorders benefit from joining a self-help or support group (telephone conference-call support groups or online support groups being of particular help for completely housebound individuals). Sharing problems and achievements with others, as well as sharing various self-help tools, are common activities in these groups. In particular, stress management techniques and various kinds of meditation practices and visualisation techniques can help people with anxiety disorders calm themselves and may enhance the effects of therapy, as can service to others, which can distract from the self-absorption that tends to go with anxiety problems. Also, preliminary evidence suggests aerobic exercise may have a calming effect. Since caffeine, certain illicit drugs, and even some over-the-counter cold medications can aggravate the symptoms of anxiety disorders, they should be avoided.

Epidemiology

Agoraphobia occurs about twice as commonly among women as it does in men.

Panic disorder with or without agoraphobia affects roughly 5.1% of Americans, and about one-third (1/3) of this population with panic disorder have co-morbid agoraphobia. It is uncommon to have agoraphobia without panic attacks, with only 0.17% of people with agoraphobia not presenting panic disorders as well.

Society and Culture

Notable Cases

  • Woody Allen (b. 1935), American actor, director, musician.
  • Kim Basinger (b. 1953), American actress.
  • Earl Campbell (b. 1955), American pro football player.
  • Macaulay Culkin (b. 1980), American actor, known for his portrayal of Kevin McCallister in Home Alone and Home Alone 2: Lost in New York, said he had “self-diagnosed” agoraphobia.
  • Paula Deen (b. 1947), American chef, author, and television personality.
  • H.L. Gold (1914-1996), science fiction editor: As a result of trauma during his wartime experiences, his agoraphobia became so severe that for more than two decades he was unable to leave his apartment. Towards the end of his life, he acquired some control over the condition.
  • Daryl Hannah (b. 1960), American actress.
  • Howard Hughes (1905-1976), American aviator, industrialist, film producer and philanthropist.
  • Olivia Hussey (b. 1951), Anglo-Argentine actress.
  • Shirley Jackson (1916-1965), American writer: Her agoraphobia is considered to be a primary inspiration for the novel We Have Always Lived in the Castle.
  • Elfriede Jelinek (b. 1946), Austrian writer, Nobel Prize laureate in Literature in 2004.
  • Bolesław Prus (1847-1912), Polish journalist and novelist.
  • Peter Robinson (b. 1962), British musician known as Marilyn.
  • Brian Wilson (b. 1942), American singer and songwriter, primary songwriter of the Beach Boys, a former recluse and agoraphobic who has schizophrenia.
  • Ben Weasel, singer and songwriter.

What is Scopophobia?

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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 Metacognitive Therapy?

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Introduction

Metacognitive therapy (MCT) is a psychotherapy focused on modifying metacognitive beliefs that perpetuate states of worry, rumination and attention fixation.

It was created by Adrian Wells based on an information processing model by Wells and Gerald Matthews. It is supported by scientific evidence from a large number of studies.

The goals of MCT are first to discover what patients believe about their own thoughts and about how their mind works (called metacognitive beliefs), then to show the patient how these beliefs lead to unhelpful responses to thoughts that serve to unintentionally prolong or worsen symptoms, and finally to provide alternative ways of responding to thoughts in order to allow a reduction of symptoms. In clinical practice, MCT is most commonly used for treating anxiety disorders such as social anxiety disorder, generalised anxiety disorder (GAD), health anxiety, obsessive compulsive disorder (OCD) and post-traumatic stress disorder (PTSD) as well as depression – though the model was designed to be transdiagnostic (meaning it focuses on common psychological factors thought to maintain all psychological disorders).

Refer to Metacognitive Training.

Brief History

Metacognition, Greek for “after” (meta) “thought” (cognition), refers to the human capacity to be aware of and control one’s own thoughts and internal mental processes. Metacognition has been studied for several decades by researchers, originally as part of developmental psychology and neuropsychology. Examples of metacognition include a person knowing what thoughts are currently in their mind and knowing where the focus of their attention is, and a person’s beliefs about their own thoughts (which may or may not be accurate). The first metacognitive interventions were devised for children with attentional disorders in the 1980s.

Model of Mental Disorders

Self-Regulatory Executive Function Model

In the metacognitive model, symptoms are caused by a set of psychological processes called the cognitive attentional syndrome (CAS). The CAS includes three main processes, each of which constitutes extended thinking in response to negative thoughts. These three processes are:

  • Worry/rumination.
  • Threat monitoring.
  • Coping behaviours that backfire.

All three are driven by patients’ metacognitive beliefs, such as the belief that these processes will help to solve problems, although the processes all ultimately have the unintentional consequence of prolonging distress. Of particular importance in the model are negative metacognitive beliefs, especially those concerning the uncontrollability and dangerousness of some thoughts. Executive functions are also believed to play a part in how the person can focus and refocus on certain thoughts and mental modes. These mental modes can be categorised as object mode and metacognitive mode, which refers to the different types of relationships people can have towards thoughts. All of the CAS, the metacognitive beliefs, the mental modes and the executive function together constitute the self-regulatory executive function model (S-REF). This is also known as the metacognitive model. In more recent work, Wells has described in greater detail a metacognitive control system of the S-REF aimed at advancing research and treatment using metacognitive therapy.

Therapeutic Intervention

MCT is a time-limited therapy which usually takes place between 8-12 sessions. The therapist uses discussions with the patient to discover their metacognitive beliefs, experiences and strategies. The therapist then shares the model with the patient, pointing out how their particular symptoms are caused and maintained.

Therapy then proceeds with the introduction of techniques tailored to the patient’s difficulties aimed at changing how the patient relates to thoughts and that bring extended thinking under control. Experiments are used to challenge metacognitive beliefs (e.g. “You believe that if you worry too much you will go ‘mad’ – let’s try worrying as much as possible for the next five minutes and see if there is any effect”) and strategies such as attentional training technique and detached mindfulness (this is a distinct strategy from various other mindfulness techniques).

Research

Clinical trials (including randomised controlled trials) have found MCT to produce large clinically significant improvements across a range of mental health disorders, although as of 2014 the total number of subjects studied is small and a meta-analysis concluded that further study is needed before strong conclusions can be drawn regarding effectiveness. A 2015 special issue of the journal Cognitive Therapy and Research was devoted to MCT research findings.

A 2018 meta-analysis confirmed the effectiveness of MCT in the treatment of a variety of psychological complaints with depression and anxiety showing high effect sizes. It concluded (Morina & Normann, 2018):

“Our findings indicate that MCT is an effective treatment for a range of psychological complaints. To date, strongest evidence exists for anxiety and depression. Current results suggest that MCT may be superior to other psychotherapies, including cognitive behavioral interventions. However, more trials with larger number of participants are needed in order to draw firm conclusions.”

In 2020, a study showed superior effectiveness in MCT over CBT in the treatment of depression. It summarised (Callesen et al., 2020):

“MCT appears promising and might offer a necessary advance in depression treatment, but there is insufficient evidence at present from adequately powered trials to assess the relative efficacy of MCT compared with CBT in depression.”

In 2018-2020, a research topic in the journal Frontiers in Psychology highlighted the growing experimental, clinical, and neuropsychological evidence base for MCT.

References

Morina, N. & Normann, N. (2018) The Efficacy of Metacognitive Therapy: A Systematic Review and Meta-Analysis. Frontiers in Psychology. 9:2211. doi:10.3389/fpsyg.2018.02211.

Callesen, P., Reeves, D., Heal, C. & Wells, A. (2020) Metacognitive Therapy versus Cognitive Behaviour Therapy in Adults with Major Depression: A Parallel Single-Blind Randomised Trial. Scientific Reports. 10(1):7878.

What is Tranylcypromine?

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Introduction

Tranylcypromine (sold under the trade name Parnate among others) is a monoamine oxidase inhibitor (MAOI); more specifically, tranylcypromine acts as nonselective and irreversible inhibitor of the enzyme monoamine oxidase (MAO).

It is used as an antidepressant and anxiolytic agent in the clinical treatment of mood and anxiety disorders, respectively.

Tranylcypromine is a propylamine formed from the cyclisation of amphetamine’s side chain; therefore, it is classified as a substituted amphetamine.

Brief History

Tranylcypromine was originally developed as an analogue of amphetamine. Although it was first synthesized in 1948, its MAOI action was not discovered until 1959. Precisely because tranylcypromine was not, like isoniazid and iproniazid, a hydrazine derivative, its clinical interest increased enormously, as it was thought it might have a more acceptable therapeutic index than previous MAOIs.

The drug was introduced by Smith, Kline and French in the United Kingdom in 1960, and approved in the United States in 1961. It was withdrawn from the market in February 1964 due to a number of patient deaths involving hypertensive crises with intracranial bleeding. However, it was reintroduced later that year with more limited indications and specific warnings of the risks.

Medical Uses

Tranylcypromine is used to treat major depressive disorder, including atypical depression, especially when there is an anxiety component, typically as a second-line treatment. It is also used in depression that is not responsive to reuptake inhibitor antidepressants, such as the SSRIs, TCAs, or bupropion.

Contraindications

Contraindications include:

  • Porphyria.
  • Cardiovascular or cerebrovascular disease.
  • Pheochromocytoma.
  • Tyramine, found in several foods, is metabolized by MAO. Ingestion and absorption of tyramine causes extensive release of norepinephrine, which can rapidly increase blood pressure to the point of causing hypertensive crisis.
  • Concomitant use of serotonin-enhancing drugs, including SSRIs, serotonergic TCAs, dextromethorphan, and meperidine may cause serotonin syndrome.
  • Concomitant use of MRAs, including fenfluramine, amphetamine, and pseudoephedrine may cause toxicity via serotonin syndrome or hypertensive crisis.
  • L-DOPA given without carbidopa may cause hypertensive crisis.

Dietary Restrictions

Tyramine is a common component in many foods, and is normally rapidly metabolised by MAO-A. Individuals not taking MAOIs may consume at least 2 grams of tyramine in a meal and not experience an increase in blood pressure, whereas those taking MAOIs such as tranylcypromine may experience a sharp increase in blood pressure following consumption of as little as 10 mg of tyramine, which can lead to hypertensive crisis.

Foods containing tyramine include aged cheeses, cured meats, tofu and certain red wines. Some, such as yeast extracts, contain enough tyramine to be potentially fatal in a single serving. Spoiled food is also likely to contain dangerous levels of tyramine.

Adverse Effects

Incidence of Adverse Effects

  • Very common (>10% incidence) adverse effects include:
    • Dizziness secondary to orthostatic hypotension (17%).
  • Common (1-10% incidence) adverse effects include:
    • Tachycardia (5-10%).
    • Hypomania (7%).
    • Paresthesia (5%).
    • Weight loss (2%).
    • Confusion (2%).
    • Dry mouth (2%).
    • Sexual function disorders (2%).
    • Hypertension (1-2 hours after ingestion) (2%).
    • Rash (2%).
    • Urinary retention (2%).
  • Other (unknown incidence) adverse effects include:
    • Increased/decreased appetite.
    • Blood dyscrasias.
    • Chest pain.
    • Diarrhoea.
    • Oedema.
    • Hallucinations.
    • Hyperreflexia.
    • Insomnia.
    • Jaundice.
    • Leg cramps.
    • Myalgia.
    • Palpitations.
    • Sensation of cold.
    • Suicidal ideation.
    • Tremor.

Of note, there has not been found to be a correlation between sex and age below 65 regarding incidence of adverse effects.

Tranylcypromine is not associated with weight gain and has a low risk for hepatotoxicity compared to the hydrazine MAOIs.

It is generally recommended that MAOIs be discontinued prior to anaesthesia; however, this creates a risk of recurrent depression. In a retrospective observational cohort study, patients on tranylcypromine undergoing general anaesthesia had a lower incidence of intraoperative hypotension, while there was no difference between patients not taking an MAOI regarding intraoperative incidence of bradycardia, tachycardia, or hypertension. The use of indirect sympathomimetic drugs or drugs affecting serotonin reuptake, such as meperidine or dextromethorphan poses a risk for hypertension and serotonin syndrome respectively; alternative agents are recommended. Other studies have come to similar conclusions. Pharmacokinetic interactions with anaesthetics are unlikely, given that tranylcypromine is a high-affinity substrate for CYP2A6 and does not inhibit CYP enzymes at therapeutic concentrations.

Tranylcypromine abuse has been reported at doses ranging from 120-600 mg per day. It is thought that higher doses have more amphetamine-like effects and abuse is promoted by the fast onset and short half-life of tranylcypromine.

Cases of suicidal ideation and suicidal behaviours have been reported during tranylcypromine therapy or early after treatment discontinuation.

Symptoms of tranylcypromine overdose are generally more intense manifestations of its usual effects.

Interactions

In addition to contraindicated concomitant medications, tranylcypromine inhibits CYP2A6, which may reduce the metabolism and increase the toxicity of substrates of this enzyme, such as:

  • Dexmedetomidine.
  • Nicotine.
  • TSNAs (found in cured tobacco products, including cigarettes).
  • Valproate.

Norepinephrine reuptake inhibitors prevent neuronal uptake of tyramine and may reduce its pressor effects.

Pharmacology

Pharmacodynamics

Tranylcypromine acts as a nonselective and irreversible inhibitor of monoamine oxidase. Regarding the isoforms of monoamine oxidase, it shows slight preference for the MAOB isoenzyme over MAOA. This leads to an increase in the availability of monoamines, such as serotonin, norepinephrine, and dopamine, as well as a marked increase in the availability of trace amines, such as tryptamine, octopamine, and phenethylamine. The clinical relevance of increased trace amine availability is unclear.

It may also act as a norepinephrine reuptake inhibitor at higher therapeutic doses. Compared to amphetamine, tranylcypromine shows low potency as a dopamine releasing agent, with even weaker potency for norepinephrine and serotonin release.

Tranylcypromine has also been shown to inhibit the histone demethylase, BHC110/LSD1. Tranylcypromine inhibits this enzyme with an IC50 < 2 μM, thus acting as a small molecule inhibitor of histone demethylation with an effect to de-repress the transcriptional activity of BHC110/LSD1 target genes. The clinical relevance of this effect is unknown.

Tranylcypromine has been found to inhibit CYP46A1 at nanomolar concentrations. The clinical relevance of this effect is unknown.

Pharmacokinetics

Tranylcypromine reaches its maximum concentration (tmax) within 1-2 hours. After a 20 mg dose, plasma concentrations reach at most 50-200 ng/mL. While its half-life is only about 2 hours, its pharmacodynamic effects last several days to weeks due to irreversible inhibition of MAO.

Metabolites of tranylcypromine include 4-hydroxytranylcypromine, N-acetyltranylcypromine, and N-acetyl-4-hydroxytranylcypromine, which are less potent MAO inhibitors than tranylcypromine itself. Amphetamine was once thought to be a metabolite of tranylcypromine, but has not been shown to be.

Tranylcypromine inhibits CYP2A6 at therapeutic concentrations.

Research

Tranylcypromine is known to inhibit LSD1, an enzyme that selectively demethylates two lysines found on histone H3. Genes promoted downstream of LSD1 are involved in cancer cell growth and metastasis, and several tumour cells express high levels of LSD1. Tranylcypromine analogues with more potent and selective LSD1 inhibitory activity are being researched in the potential treatment of cancers.

Tranylcypromine may have neuroprotective properties applicable to the treatment of Parkinson’s disease, similar to the MAO-B inhibitors selegiline and rasagiline. As of 2017, only one clinical trial in Parkinsonian patients has been conducted, which found some improvement initially and only slight worsening of symptoms after a 1.5 year follow-up.

What is the Gut-Brain Axis?

Published on by Andrew Marshall1 Comment

Introduction

The gut-brain axis is the biochemical signalling that takes place between the gastrointestinal tract (GI tract) and the central nervous system (CNS).

The term “gut-brain axis” is occasionally used to refer to the role of the gut flora in the interplay as well, whereas the term “microbiota–gut–brain (MGB or BGM) axis” explicitly includes the role of gut flora in the biochemical signalling events that take place between the GI tract and CNS.

Broadly defined, the gut-brain axis includes the central nervous system, neuroendocrine and neuroimmune systems, including the hypothalamic-pituitary-adrenal axis (HPA axis), sympathetic and parasympathetic arms of the autonomic nervous system, including the enteric nervous system and the vagus nerve, and the gut microbiota. The first of the brain-gut interactions shown, was the cephalic phase of digestion, in the release of gastric and pancreatic secretions in response to sensory signals, such as the smell and sight of food. This was first demonstrated by Pavlov.

Interest in the field was sparked by a 2004 study showing that germ-free (GF) mice showed an exaggerated HPA axis response to stress compared to non-GF laboratory mice.

As of October 2016, most of the work done on the role of gut flora in the gut-brain axis had been conducted in animals, or on characterising the various neuroactive compounds that gut flora can produce. Studies with humans – measuring variations in gut flora between people with various psychiatric and neurological conditions or when stressed, or measuring effects of various probiotics (dubbed “psychobiotics” in this context) – had generally been small and were just beginning to be generalised. Whether changes to gut flora are a result of disease, a cause of disease, or both in any number of possible feedback loops in the gut–brain axis, remained unclear.

Gut Flora

The gut flora is the complex community of microorganisms that live in the digestive tracts of humans and other animals. The gut metagenome is the aggregate of all the genomes of gut microbiota. The gut is one niche that human microbiota inhabit.

In humans, the gut microbiota has the largest quantity of bacteria and the greatest number of species, compared to other areas of the body. In humans, the gut flora is established at one to two years after birth; by that time, the intestinal epithelium and the intestinal mucosal barrier that it secretes have co-developed in a way that is tolerant to, and even supportive of, the gut flora and that also provides a barrier to pathogenic organisms.

The relationship between gut flora and humans is not merely commensal (a non-harmful coexistence), but rather a mutualistic relationship. Human gut microorganisms benefit the host by collecting the energy from the fermentation of undigested carbohydrates and the subsequent absorption of short-chain fatty acids (SCFAs), acetate, butyrate, and propionate. Intestinal bacteria also play a role in synthesizing vitamin B and vitamin K as well as metabolising bile acids, sterols, and xenobiotics. The systemic importance of the SCFAs and other compounds they produce are like hormones and the gut flora itself appears to function like an endocrine organ; dysregulation of the gut flora has been correlated with a host of inflammatory and autoimmune conditions.

The composition of human gut flora changes over time, when the diet changes, and as overall health changes.

Enteric Nervous System

The enteric nervous system is one of the main divisions of the nervous system and consists of a mesh-like system of neurons that governs the function of the gastrointestinal system; it has been described as a “second brain” for several reasons. The enteric nervous system can operate autonomously. It normally communicates with the central nervous system (CNS) through the parasympathetic (e.g. via the vagus nerve) and sympathetic (e.g. via the prevertebral ganglia) nervous systems. However, vertebrate studies show that when the vagus nerve is severed, the enteric nervous system continues to function.

In vertebrates, the enteric nervous system includes efferent neurons, afferent neurons, and interneurons, all of which make the enteric nervous system capable of carrying reflexes in the absence of CNS input. The sensory neurons report on mechanical and chemical conditions. Through intestinal muscles, the motor neurons control peristalsis and churning of intestinal contents. Other neurons control the secretion of enzymes. The enteric nervous system also makes use of more than 30 neurotransmitters, most of which are identical to the ones found in CNS, such as acetylcholine, dopamine, and serotonin. More than 90% of the body’s serotonin lies in the gut, as well as about 50% of the body’s dopamine; the dual function of these neurotransmitters is an active part of gut-brain research.

The first of the gut-brain interactions was shown to be between the sight and smell of food and the release of gastric secretions, known as the cephalic phase, or cephalic response of digestion.

Gut-Brain Integration

The gut-brain axis, a bidirectional neurohumoral communication system, is important for maintaining homeostasis and is regulated through the central and enteric nervous systems and the neural, endocrine, immune, and metabolic pathways, and especially including the hypothalamic-pituitary-adrenal axis (HPA axis). That term has been expanded to include the role of the gut flora as part of the “microbiome-gut-brain axis”, a linkage of functions including the gut flora.

Interest in the field was sparked by a 2004 study (Nobuyuki Sudo and Yoichi Chida) showing that germ-free mice (genetically homogeneous laboratory mice, birthed and raised in an antiseptic environment) showed an exaggerated HPA axis response to stress, compared to non-GF laboratory mice.

The gut flora can produce a range of neuroactive molecules, such as acetylcholine, catecholamines, γ-aminobutyric acid, histamine, melatonin, and serotonin, which are essential for regulating peristalsis and sensation in the gut. Changes in the composition of the gut flora due to diet, drugs, or disease correlate with changes in levels of circulating cytokines, some of which can affect brain function. The gut flora also release molecules that can directly activate the vagus nerve, which transmits information about the state of the intestines to the brain.

Likewise, chronic or acutely stressful situations activate the hypothalamic-pituitary-adrenal axis, causing changes in the gut flora and intestinal epithelium, and possibly having systemic effects. Additionally, the cholinergic anti-inflammatory pathway, signalling through the vagus nerve, affects the gut epithelium and flora. Hunger and satiety are integrated in the brain, and the presence or absence of food in the gut and types of food present also affect the composition and activity of gut flora.

That said, most of the work that has been done on the role of gut flora in the gut-brain axis has been conducted in animals, including the highly artificial germ-free mice. As of 2016, studies with humans measuring changes to gut flora in response to stress, or measuring effects of various probiotics, have generally been small and cannot be generalised; whether changes to gut flora are a result of disease, a cause of disease, or both in any number of possible feedback loops in the gut-brain axis, remains unclear.

The history of ideas about a relationship between the gut and the mind dates from the nineteenth century. The concepts of dyspepsia and neurasthenia gastrica referred to the influence of the gut on human emotions and thoughts.

Gut-Brain-Skin Axis

A unifying theory that tied gastrointestinal mechanisms to anxiety, depression, and skin conditions such as acne was proposed as early as 1930. In a paper in 1930, it was proposed that emotional states might alter normal intestinal flora which could lead to increased intestinal permeability and therefore contribute to systemic inflammation. Many aspects of this theory have been validated since then. Gut microbiota and oral probiotics have been found to influence systemic inflammation, oxidative stress, glycaemic control, tissue lipid content, and mood.

Research

Probiotics

A 2016 systematic review of laboratory animal studies and preliminary human clinical trials using commercially available strains of probiotic bacteria found that certain species of the Bifidobacterium and Lactobacillus genera (i.e. B. longum, B. breve, B. infantis, L. helveticus, L. rhamnosus, L. plantarum, and L. casei) had the most potential to be useful for certain central nervous system disorders.

Anxiety and Mood Disorders

As of 2018 work on the relationship between gut flora and anxiety disorders and mood disorders, as well as attempts to influence that relationship using probiotics or prebiotics (called “psychobiotics”), was at an early stage, with insufficient evidence to draw conclusions about a causal role for gut flora changes in these conditions, or about the efficacy of any probiotic or prebiotic treatment.

People with anxiety and mood disorders tend to have gastrointestinal problems; small studies have been conducted to compare the gut flora of people with major depressive disorder and healthy people, but those studies have had contradictory results.

Much interest was generated in the potential role of gut flora in anxiety disorders, and more generally in the role of gut flora in the gut-brain axis, by studies published in 2004 showing that germ-free mice have an exaggerated HPA axis response to stress caused by being restrained, which was reversed by colonising their gut with a Bifidobacterium species. Studies looking at maternal separation for rats shows neonatal stress leads to long-term changes in the gut microbiota such as its diversity and composition, which also led to stress and anxiety-like behaviour. Additionally, while much work had been done as of 2016 to characterise various neurotransmitters known to be involved in anxiety and mood disorders that gut flora can produce (for example, Escherichia, Bacillus, and Saccharomyces species can produce noradrenalin; Candida, Streptococcus, and Escherichia species can produce serotonin, etc.) the interrelationships and pathways by which the gut flora might affect anxiety in humans were unclear.

In one study, germ-free mice underwent faecal transplants with microbes from humans with or without major depressive disorder (MDD). Mice with microbes from humans with MDD displayed more behaviours associated with anxiety and depression than mice transplanted with microbes from humans without MDD. The taxonomic composition of microbiota between depressed patients and healthy patients, as well as between the respective mice, also differed. Germ-free mice in another study also displayed behaviours associated with anxiety and depression as compared to mice with normal microbiota, and had higher levels of corticosterone after exposure to behavioural tests. Using rodents in microbiome and mental health studies allows researchers to compare behaviour and microbial composition of rodents to humans, ideally to elucidate therapeutic application for mental disorders.

Additionally, there is a link between the gut microbiome, mood disorders and anxiety, and sleep. The microbial composition of the gut microbiome changes depending on the time of day, meaning that throughout the day, the gut is exposed to varying metabolites produced by the microbes active during that time. These time-dependent microbial changes are associated with differences in the transcription of circadian clock genes involved in circadian rhythm. One mouse study showed that altering clock gene transcription by disrupting circadian rhythm, such as through sleep deprivation, potentially has a direct effect on the composition of the gut microbiome. Another study found that mice that could not produce the CLOCK protein, made by a clock gene, were more likely to develop depression. Stress and sleep disturbances can lead to greater gut mucosal permeability via activation of the HPA axis. This in turn causes immune inflammatory responses that contribute to the development of illnesses that cause depression and anxiety.

Autism

Around 70% of people with autism also have gastrointestinal problems, and autism is often diagnosed at the time that the gut flora becomes established, indicating that there may be a connection between autism and gut flora. Some studies have found differences in the gut flora of children with autism compared with children without autism – most notably elevations in the amount of Clostridium in the stools of children with autism compared with the stools of the children without – but these results have not been consistently replicated. Many of the environmental factors thought to be relevant to the development of autism would also affect the gut flora, leaving open the question of whether specific developments in the gut flora drive the development of autism or whether those developments happen concurrently. As of 2016, studies with probiotics had only been conducted with animals; studies of other dietary changes to treat autism have been inconclusive.

Parkinson’s Disease

As of 2015, one study had been conducted comparing the gut flora of people with Parkinson’s disease to healthy controls; in that study people with Parkinson’s had lower levels of Prevotellaceae and people with Parkinson’s who had higher levels of Enterobacteriaceae had more clinically severe symptoms; the authors of the study drew no conclusions about whether gut flora changes were driving the disease or vice versa.

Can the MHS: A Serve as a Clinically Useful Screening Tool for GAD?

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Research Paper Title

A Brief Online and Offline (Paper-and-Pencil) Screening Tool for Generalized Anxiety Disorder: The Final Phase in the Development and Validation of the Mental Health Screening Tool for Anxiety Disorders (MHS: A).

Background

Generalised anxiety disorder (GAD) can cause significant socioeconomic burden and daily life dysfunction; hence, therapeutic intervention through early detection is important.

Methods

This study was the final stage of a 3-year anxiety screening tool development project that evaluated the psychometric properties and diagnostic screening utility of the Mental Health Screening Tool for Anxiety Disorders (MHS: A), which measures GAD.

Results

A total of 527 Koreans completed online and offline (i.e., paper-and pencil) versions of the MHS: A, Beck Anxiety Inventory (BAI), Generalised Anxiety Disorder-7 (GAD-7), and Penn State Worry Questionnaire (PSWQ). The participants had an average age of 38.6 years and included 340 (64.5%) females. Participants were also administered the Mini-International Neuropsychiatric Interview (MINI).

Internal consistency, convergent/criterion validity, item characteristics, and test information were assessed based on the item response theory (IRT), and a factor analysis and cut-off score analyses were conducted. The MHS: A had good internal consistency and good convergent validity with other anxiety scales.

The two versions (online/offline) of the MHS: A were nearly identical (r = 0.908). It had a one-factor structure and showed better diagnostic accuracy (online/offline: sensitivity = 0.98/0.90, specificity = 0.80/0.83) for GAD detection than the GAD-7 and BAI. The IRT analysis indicated that the MHS: A was most informative as a screening tool for GAD.

Conclusions

The MHS: A can serve as a clinically useful screening tool for GAD in Korea. Furthermore, it can be administered both online and offline and can be flexibly used as a brief mental health screener, especially with the current rise in telehealth.

Reference

Kim, S-H., Park, K., Yoon, S., Choi, Y., Lee, S-H. & Choi, K-H. (2021) A Brief Online and Offline (Paper-and-Pencil) Screening Tool for Generalized Anxiety Disorder: The Final Phase in the Development and Validation of the Mental Health Screening Tool for Anxiety Disorders (MHS: A). Frontiers in Psychology. doi: 10.3389/fpsyg.2021.639366. eCollection 2021.

Anxiety Youth vs Healthy Youth: Threat-Anticipatory Psychophysiological Response Differences

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Research Paper Title

Threat-anticipatory psychophysiological response is enhanced in youth with anxiety disorders and correlates with prefrontal cortex neuroanatomy.

Background

Threat anticipation engages neural circuitry that has evolved to promote defensive behaviours; perturbations in this circuitry could generate excessive threat-anticipation response, a key characteristic of pathological anxiety. Research into such mechanisms in youth faces ethical and practical limitations. Here, the researchers use thermal stimulation to elicit pain-anticipatory psychophysiological response and map its correlates to brain structure among youth with anxiety and healthy youth.

Methods

Youth with anxiety (n = 25) and healthy youth (n = 25) completed an instructed threat-anticipation task in which cues predicted nonpainful or painful thermal stimulation; the researchers indexed psychophysiological response during the anticipation and experience of pain using skin conductance response. High-resolution brain-structure imaging data collected in another visit were available for 41 participants. Analyses tested whether the 2 groups differed in their psychophysiological cue-based pain-anticipatory and pain-experience responses. Analyses then mapped psychophysiological response magnitude to brain structure.

Results

Youth with anxiety showed enhanced psychophysiological response specifically during anticipation of painful stimulation (b = 0.52, p = 0.003). Across the sample, the magnitude of psychophysiological anticipatory response correlated negatively with the thickness of the dorsolateral prefrontal cortex (pFWE < 0.05); psychophysiological response to the thermal stimulation correlated positively with the thickness of the posterior insula (pFWE < 0.05).

Limitations: Limitations included the modest sample size and the cross-sectional design.

Conclusions

These findings show that threat-anticipatory psychophysiological response differentiates youth with anxiety from healthy youth, and they link brain structure to psychophysiological response during pain anticipation and experience. A focus on threat anticipation in research on anxiety could delineate relevant neural circuitry.

Reference

Abend, R., Bajaj, M.A., Harrwijn, A., Matsumoto, C., Michalska, K.J., Necka, E., Palacios-Barrios, E.E., Leibenluft, E., Atlas, L.Y. & Pine, D.S. (2021) Threat-anticipatory psychophysiological response is enhanced in youth with anxiety disorders and correlates with prefrontal cortex neuroanatomy. Journal of Psychiatry & Neuroscience. 46(2):E212-E221. doi: 10.1503/jpn.200110.

Book: CBT Journal for Dummies

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Book Title:

CBT Journal for Dummies.

Author(s): Rob Wilson and Rhena Branch.

Year: 2012.

Edition: First (1st).

Publisher: Wiley.

Type(s): Hardcover.

Synopsis:

Keep track of the progress you are making with Cognitive Behavioural Therapy.

Cognitive Behavioural Therapy (CBT) is a hugely popular self-help technique that teaches you how to break free from destructive or negative behaviours and make positive changes to both your thoughts and your actions. CBT Journal For Dummies offers a guided space for you to keep a record of your progress, used in conjunction with either CBT For Dummies and/or alongside consultation with a therapist.

This book features an introduction to CBT, followed by a guided 100-day journal. Each chapter focuses on a new CBT technique, with information on how to use the journal space and assessment advice. Topics covered include; establishing the link between thoughts and feelings; preventing ‘all or nothing’ thinking; turning mountains into molehills; focusing on the present; using emotional reasoning; avoiding over-generalising; thinking flexibly; keeping an open mind; assessing the positives; coping with frustration; tackling toxic thoughts; naming your emotions; comparing healthy and unhealthy emotions; working through worry; defining your core beliefs; adopting positive principles; and much more.

  • Has a removable band, leaving a discreet black journal.
  • The small trim size makes it perfect to use on the go.
  • A CBT ‘thought for the day’ appears on alternate blank pages.
  • Content is progressive, encouraging you to keep working through the following days.
  • Coverage is generalized enough to be applicable to every user of CBT.

Book: Managing Anxiety with CBT for Dummies

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Book Title:

Managing Anxiety with CBT for Dummies.

Author(s): Graham C. Davey, Kate Cavanagh, Fergal Jones, Lydia Turner, and Adrian Whittington.

Year: 2012.

Edition: First (1st).

Publisher: Wiley.

Type(s): Paperback, Audiobook, and Kindle.

Synopsis:

Don’t panic! Combat your worries and minimise anxiety with CBT!
Cognitive Behavioural Therapy (CBT) is a hugely popular self-help technique, which teaches you to break free from destructive or negative behaviours and make positive changes to both your thoughts and your actions. This practical guide to managing anxiety with CBT will help you understand your anxiety, identify solutions to your problems, and maintain your gains and avoid relapse.

Managing Anxiety with CBT For Dummies is a practical guide to using CBT to face your fears and overcome anxiety and persistent, irrational worries. You’ll discover how to put extreme thinking into perspective and challenge negative, anxiety-inducing thoughts with a range of effective CBT techniques to help you enjoy a calmer, happier life.

  • Helps you understand anxiety and how CBT can help.
  • Guides you in making change and setting goals.
  • Gives you tried-and-true CBT techniques to face your fears and keep a realistic perspective.

Managing Anxiety with CBT For Dummies gives you the tools you need to overcome anxiety and expand your horizons for a healthy, balanced life.