What is Hikikomori?

Introduction

Hikikomori (Japanese: ひきこもり or 引き籠もり, lit. “pulling inward, being confined”), also known as “acute social withdrawal” , is total withdrawal from society and seeking extreme degrees of social isolation and confinement. Hikikomori refers to both the phenomenon in general and the recluses themselves. Hikikomori have been described as loners or “modern-day hermits”. Estimates suggest that half a million Japanese youths have become social recluses, as well as more than half a million middle-aged individuals.

Definition

The Japanese Ministry of Health, Labour, and Welfare defines hikikomori as a condition in which the affected individuals refuse to leave their parents’ house, do not work or go to school and isolate themselves away from society and family in a single room for a period exceeding six months. The psychiatrist Tamaki Saitō defines hikikomori as “a state that has become a problem by the late twenties, that involves cooping oneself up in one’s own home and not participating in society for six months or longer, but that does not seem to have another psychological problem as its principal source”.

More recently, researchers have developed more specific criteria to more accurately identify hikikomori. During a diagnostic interview, trained clinicians evaluate for:

  • Spending most of the day and nearly every day confined to home;
  • Marked and persistent avoidance of social situations, and social relationships;
  • Social withdrawal symptoms causing significant functional impairment;
  • Duration of at least six months; and
  • No apparent physical or mental aetiology to account for the social withdrawal symptoms.

The psychiatrist Alan Teo first characterised hikikomori in Japan as modern-day hermits, while the literary and communication scholar Flavio Rizzo similarly described hikikomori as “post-modern hermits” whose solitude stems from ancestral desires for withdrawal.

While the degree of the phenomenon varies on an individual basis, in the most extreme cases, some people remain in isolation for years or even decades. Often hikikomori start out as school refusers, or futōkō (不登校) in Japanese (an older term is tōkōkyohi (登校拒否)).

Common Traits

While many people feel the pressures of the outside world, hikikomori react by complete social withdrawal. In some more extreme cases, they isolate themselves in their bedrooms for months or years at a time. They usually have few or no friends. In interviews with current or recovering hikikomori, media reports and documentaries have captured the strong levels of psychological distress and angst felt by these individuals.

While hikikomori favour indoor activities, some venture outdoors occasionally. The withdrawal from society usually starts gradually. Affected people may appear unhappy, lose their friends, become insecure and shy, and talk less.

Prevalence

According to Japanese government figures released in 2010, there are 700,000 individuals living as hikikomori within Japan, with an average age of 31. Still, the numbers vary widely among experts. These include the hikikomori who are now in their 40s (as of 2011) and have spent 20 years in isolation. This group is generally referred to as the “first-generation hikikomori.” There is concern about their reintegration into society in what is known as “the 2030 Problem,” when they are in their 60s and their parents begin to die. Additionally, the government estimates that 1.55 million people are on the verge of becoming hikikomori. Tamaki Saitō, who first coined the phrase, originally estimated that there may be over one million hikikomori in Japan, although this was not based on national survey data. Nonetheless, considering that hikikomori adolescents are hidden away and their parents are often reluctant to talk about the problem, it is extremely difficult to gauge the number accurately.

A 2015 Cabinet Office survey estimated that 541,000 recluses aged 15 to 39 existed. In 2019, another survey showed that there are roughly 613,000 people aged 40 to 64 that fall into the category of “adult hikikomori”, which Japan’s welfare minister Takumi Nemoto referred to as a “new social issue.”

While hikikomori is mostly a Japanese phenomenon, cases have been found in the United States, United Kingdom, Oman, Spain, Italy, India, Sweden, South Korea, and France.

Hypotheses on the Cause(s)

Developmental and Psychiatric Conditions

Hikikomori is similar to the social withdrawal exhibited by some people with autism spectrum disorders, a group of developmental disorders that include Asperger syndrome, PDD-NOS and “classic” autism. This has led some psychiatrists to suggest that hikikomori may be affected by autism spectrum disorders and other disorders that affect social integration, but that their disorders are altered from their typical Western presentation because of Japanese sociocultural pressures. Suwa & Hara (2007) discovered that 5 of 27 cases of hikikomori had a high-functioning pervasive developmental disorder (HPDD), and 12 more had other disorders or mental diseases (6 cases of personality disorders, 3 cases of obsessive-compulsive disorder, 2 cases of depression, 1 case of slight mental retardation); 10 out of 27 had primary hikikomori. The researchers used a vignette to illustrate the difference between primary hikikomori (without any obvious mental disorder) and hikikomori with HPDD or other disorder. Alan Teo and colleagues conducted detailed diagnostic evaluations of 22 individuals with hikikomori and found that while the majority of cases fulfilled criteria for multiple psychiatric conditions, about 1 in 5 cases were primary hikikomori. Till date, however, hikikomori is not included in the DSM-5, due to insufficient data.

According to Michael Zielenziger’s book, Shutting Out the Sun: How Japan Created Its Own Lost Generation, the syndrome is more closely related to posttraumatic stress disorder. The author claimed that the hikikomori interviewed for the book had discovered independent thinking and a sense of self that the current Japanese environment could not accommodate.

The syndrome also closely parallels the terms avoidant personality disorder, schizoid personality disorder, schizotypal personality disorder, agoraphobia or social anxiety disorder (also known as “social phobia”).

Social and Cultural Influence

Sometimes referred to as a social problem in Japanese discourse, hikikomori has a number of possible contributing factors. Alan Teo has summarised a number of potential cultural features that may contribute to its predominance in Japan. These include tendencies toward conformity and collectivism, overprotective parenting, and particularities of the educational, housing and economic systems.

Acute social withdrawal in Japan appears to affect both genders equally. However, because of differing social expectations for maturing boys and girls, the most widely reported cases of hikikomori are from middle- and upper-middle-class families; sons, typically their eldest, refuse to leave the home, often after experiencing one or more traumatic episodes of social or academic failure.

In The Anatomy of Dependence, Takeo Doi identifies the symptoms of hikikomori, and explains its prevalence as originating in the Japanese psychological construct of amae (in Freudian terms, “passive object love”, typically of the kind between mother and infant). Other Japanese commentators such as academic Shinji Miyadai and novelist Ryū Murakami, have also offered analysis of the hikikomori phenomenon, and find distinct causal relationships with the modern Japanese social conditions of anomie, amae and atrophying paternal influence in nuclear family child pedagogy. Young adults may feel overwhelmed by modern Japanese society, or be unable to fulfil their expected social roles as they have not yet formulated a sense of personal honne and tatemae – one’s “true self” and one’s “public façade” – necessary to cope with the paradoxes of adulthood.

The dominant nexus of hikikomori centres on the transformation from youth to the responsibilities and expectations of adult life. Indications are that advanced industrialised societies such as modern Japan fail to provide sufficient meaningful transformation rituals for promoting certain susceptible types of youth into mature roles. As do many societies, Japan exerts a great deal of pressure on adolescents to be successful and perpetuate the existing social status quo. A traditionally strong emphasis on complex social conduct, rigid hierarchies and the resulting, potentially intimidating multitude of social expectations, responsibilities and duties in Japanese society contribute to this pressure on young adults. Historically, Confucian teachings de-emphasizing the individual and favouring a conformist stance to ensure social harmony in a rigidly hierarchized society have shaped much of East Asia, possibly explaining the emergence of the hikikomori phenomenon in other East Asian countries.

In general, the prevalence of hikikomori tendencies in Japan may be encouraged and facilitated by three primary factors:

  • Middle class affluence in a post-industrial society such as Japan allows parents to support and feed an adult child in the home indefinitely.
    • Lower-income families do not have hikikomori children because a socially withdrawing youth is forced to work outside the home.
  • The inability of Japanese parents to recognise and act upon the youth’s slide into isolation; soft parenting; or co-dependence between mother and son, known as amae in Japanese.
  • A decade of flat economic indicators and a shaky job market in Japan makes the pre-existing system requiring years of competitive schooling for elite jobs appear like a pointless effort to many.

Role of Modern Technology

Although the connection between modern communication technologies, such as the Internet, social media and video games, and the phenomenon is not conclusively established, it is considered at least an exacerbating factor that can deepen and nurture withdrawal. Previous studies of hikikomori in South Korea and Spain found that some of them showed signs of Internet addiction, though researchers do not consider this to be the main issue. However, according to associate professor of psychiatry at Kyushu University in Fukuoka, Takahiro Kato, video games and social media have reduced the amount of time that people spent outside and in social environments that require direct face to face interaction. The emergence of mobile phones and then smartphones may also have deepened the issue, given that people can continue their addiction to gaming and online surfing anywhere, even in bed.

Japanese Education System

The Japanese education system, like those found in China, Singapore, India, and South Korea, puts great demands upon youth. A multitude of expectations, high emphasis on competition, and the rote memorization of facts and figures for the purpose of passing entrance exams into the next tier of education in what could be termed a rigid pass-or-fail ideology, induce a high level of stress. Echoing the traditional Confucian values of society, the educational system is viewed as playing an important part in society’s overall productivity and success.

In this social frame, students often face significant pressure from parents and the society in general to conform to its dictates and doctrines. These doctrines, while part of modern Japanese society, are increasingly being rejected by Japanese youth in varying ways such as hikikomori, freeter, NEET (Not currently engaged in Employment, Education, or Training), and parasite singles. The term “Hodo-Hodo zoku” (the “So-So tribe”) applies to younger workers who refuse promotion to minimise stress and maximise free time.

Beginning in the 1960s, the pressure on Japanese youth to succeed began successively earlier in their lives, sometimes starting before pre-school, where even toddlers had to compete through an entrance exam for the privilege of attending one of the best pre-schools. This was said to prepare children for the entrance exam of the best kindergarten, which in turn prepared the child for the entrance exam of the best elementary school, junior high school, high school, and eventually for their university entrance exam. Many adolescents take one year off after high school to study exclusively for the university entrance exam, and are known as ronin. More prestigious universities have more difficult exams. The most prestigious university with the most difficult exam is the University of Tokyo.

Since 1996, the Japanese Ministry of Education has taken steps to address this ‘pressure-cooker’ educational environment and instil greater creative thought in Japanese youth by significantly relaxing the school schedule from six-day weeks to five-day weeks and dropping two subjects from the daily schedule, with new academic curricula more comparable to Western educational models. However, Japanese parents are sending their children to private cram schools, known as juku, to ‘make up’ for lost time.

After graduating from high school or university, Japanese youth also have to face a very difficult job market in Japan, often finding only part-time employment and ending up as freeters with little income, unable to start a family.

Another source of pressure is from their co-students, who may harass and bully (ijime) some students for a variety of reasons, including physical appearance, wealth, or educational or athletic performance. Some have been punished for bullying or truancy, bringing shame to their families. Refusal to participate in society makes hikikomori an extreme subset of a much larger group of younger Japanese that includes freeters.

Impact

Japanese Financial Burden

Some organizations such as the non-profit Japanese organisation NPO lila have been trying to combat the financial burden the hikikomori phenomenon has had on Japan’s economy. The Japanese CD and DVD producer Avex Group produces DVD videos of live-action women staring into a camera to help hikikomori learn to cope with eye contact and long spans of human interaction. The goal is to help hikikomori reintegrate into society by personal choice, thereby realising an economic contribution and reducing the financial burden on parents.

“80-50 Problem”

Described in Japanese literature and media, first from the late 2010s, hikikomori of youth from earlier days, as have their parents upon whom they rely. The “80-50 problem” refers to the hikikomori children being in their 50s (or thereabouts), with their only means of support being their ageing parents who are in their 80s (or thereabouts).

A Japanese government Cabinet Office survey counted roughly 540,000 hikikomori people in 2015. However, this survey covers a restricted age group of 15 to 39 years of age. Hikikomori people in their 40s and 50s are consequently not surveyed or otherwise studied.

In 2019, Japanese psychiatrist Dr. Saitō Tamaki held a press briefing at the Foreign Press Centre Japan on the subject of hikikomori. Among addressing ageing, he recommended practical advice to that parents with hikikomori, such as drawing up a lifetime financial plan for hikikomori children, so they can get by after the parents are gone. He also recommended that parents should not fear embarrassment or be concerned about appearances as they look at the options, including disability pensions or other forms of public assistance for their children. Given the Japanese government – failing to see the urgency of the problem – is demonstrating no motion toward developing substantive policies or systems related to the ageing of hikikomori, Dr Tamaki has emphasised the urgency and necessity for families to plan ahead.

Treatment Programmes

When it comes to psychosocial support, it is hard for therapists to attain direct access to hikikomori; research to find different and effective treatment plans to aid hikikomori has been ongoing. One such treatment plan is focused on the families of hikikomori. Such focus primarily includes, educational intervention programmes (e.g. lectures, role-play, etc.) that are geared towards reducing any averse stigma that family members have towards psychiatric disorders like hikikomori. These educational programmes are derived from other established family support programmes, specifically Mental Health First Aid (MFHA) and Community Reinforcement and Family Training (CRAFT). CRAFT specifically trains family members express positive and functional communication, whereas MFHA provides skills to support hikikomori with depression/suicidal like behaviour. Studies so far that have modified the family unit’s behavioural response to a hikikomori has yielded positive results, indicating that family behaviour is essential for recovery, however further research is still needed.

Although there has been a primary emphasis on educating family members, there are still therapy programmes for the hikikomori to participate themselves in. For example, the use of exercise therapy. The individual psychotherapy methods that are being stressed in current research are primarily motivated on cultivating self-confidence within the hikikomori. With that being said, however, studies have delineated that efficacious treatment towards hikikomori requires a multifaceted approach rather than the utilisation of one individual approach, such as individual psychotherapy or family therapy.

Pandemic Impact

Based on prior outbreaks (e.g. SARS, MERS, etc.), studies have shown that quarantined individuals, due to increased loneliness, have heightened stress-related mental disturbances. Considering that political, social, and/or economical challenges already bring people to express hikikomori like behaviour, researchers theorise that since all the aforementioned factors are by-products of a pandemic, many postulate a hikikomori phenomenon common in a post-pandemic world. In fact, people who do experience mental disturbances in Japan generally view seeking the help of a psychiatrist as shameful or a reason for them to be socially shunned. Experts predict an increase in focus on both the youth and also on mental health specifically through effective telemedicine to either the affected individual and/or their respective family unit.

Furthermore, with hikikomori becoming more prevalent amid a pandemic, experts theorise that it will bring out more empathy and constructive attention towards the issue.

What is Agoraphobia?

Introduction

Agoraphobia is 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. The symptoms occur nearly every time the situation is encountered and last for more than six months. 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. Those affected are at higher risk of depression and substance use disorder.

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. 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. The term “agoraphobia” is from Greek ἀγορά, agorā́, meaning a “place of assembly” or “market-place” and -φοβία, -phobía, meaning “fear.”

Refer to Hikikomori.

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 safe 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 (OCD) or post-traumatic stress disorder (PTSD) 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. 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 urbanization. These have helped develop the expansion of public space, on one hand, and the contraction of private space on the other, thus creating in the minds of agoraphobia-prone people a tense, unbridgeable gulf 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 CBT 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.

Medications

Antidepressant medications most commonly used to treat anxiety disorders are mainly selective serotonin reuptake inhibitors. 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 cognitive behaviour therapy 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. If taken for too long, they can cause dependence. Treatment with benzodiazepines should not exceed 4 weeks. Side effects may include confusion, drowsiness, light-headedness, loss of balance, and memory loss.

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. The gender difference may be attributable to several factors: sociocultural traditions that encourage, or permit, the greater expression of avoidance coping strategies by women (including dependent and helpless behaviours), women perhaps being more likely to seek help and therefore be diagnosed, and men being more likely to abuse alcohol in reaction to anxiety and be diagnosed as an alcoholic. Research has not yet produced a single clear explanation for the gender difference in agoraphobia.

Panic disorder with or without agoraphobia affects roughly 5.1% of Americans, and about 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.

In Popular 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.

What is Panic Disorder?

Introduction

Panic disorder is an anxiety disorder characterised by reoccurring unexpected panic attacks. Panic attacks are sudden periods of intense fear that may include palpitations, sweating, shaking, shortness of breath, numbness, or a feeling that something terrible is going to happen. The maximum degree of symptoms occurs within minutes. There may be ongoing worries about having further attacks and avoidance of places where attacks have occurred in the past.

The cause of panic disorder is unknown. Panic disorder often runs in families. Risk factors include smoking, psychological stress, and a history of child abuse. Diagnosis involves ruling out other potential causes of anxiety including other mental disorders, medical conditions such as heart disease or hyperthyroidism, and drug use. Screening for the condition may be done using a questionnaire.

Panic disorder is usually treated with counselling and medications. The type of counselling used is typically cognitive behavioural therapy (CBT) which is effective in more than half of people. Medications used include antidepressants and occasionally benzodiazepines or beta blockers. Following stopping treatment up to 30% of people have a recurrence.

Panic disorder affects about 2.5% of people at some point in their life. It usually begins during adolescence or early adulthood but any age can be affected. It is less common in children and older people. Women are more often affected than men.

Signs and Symptoms

Panic disorder sufferers usually have a series of intense episodes of extreme anxiety during panic attacks. These attacks typically last about ten minutes, and can be as short-lived as 1-5 minutes, but can last twenty minutes to more than an hour, or until helpful intervention is made. Panic attacks can wax and wane for a period of hours (panic attacks rolling into one another), and the intensity and specific symptoms of panic may vary over the duration.

In some cases, the attack may continue at unabated high intensity or seem to be increasing in severity. Common symptoms of an attack include rapid heartbeat, perspiration, dizziness, dyspnoea, trembling, uncontrollable fear such as: the fear of losing control and going crazy, the fear of dying and hyperventilation. Other symptoms are a sensation of choking, paralysis, chest pain, nausea, numbness or tingling, chills or hot flashes, faintness, crying and some sense of altered reality. In addition, the person usually has thoughts of impending doom. Individuals suffering from an episode have often a strong wish of escaping from the situation that provoked the attack. The anxiety of panic disorder is particularly severe and noticeably episodic compared to that from generalised anxiety disorder. Panic attacks may be provoked by exposure to certain stimuli (e.g. seeing a mouse) or settings (e.g. the dentist’s office). Nocturnal panic attacks are common in people with panic disorder. Other attacks may appear unprovoked. Some individuals deal with these events on a regular basis, sometimes daily or weekly.

Limited symptom attacks are similar to panic attacks but have fewer symptoms. Most people with PD experience both panic attacks and limited symptom attacks.

Interoceptive

Studies investigating the relationship between interoception and panic disorder have shown that people with panic disorder feel heartbeat sensations more intensely when stimulated by pharmacological agents, suggesting that they experience heightened interoceptive awareness compared to subjects without PD.

Causes

Psychological Models

While there is not just one explanation for the cause of panic disorder, there are certain perspectives researchers use to explain the disorder. The first one is the biological perspective. Past research concluded that there is irregular norepinephrine activity in people who have panic attacks. Current research also supports this perspective as it has been found that those with panic disorder also have a brain circuit that performs improperly. This circuit consists of the amygdala, central gray matter, ventromedial nucleus of the hypothalamus, and the locus ceruleus.

There is also a cognitive perspective. Theorists believe that people with panic disorder may experience panic reactions because they mistake their bodily sensations for life-threatening situations. These bodily sensations cause some people to feel as though are out of control which may lead to feelings of panic. This misconception of bodily sensations is referred to as anxiety sensitivity, and studies suggest that people who score higher on anxiety sensitivity surveys are fives times more likely to be diagnosed with panic disorder.

Panic disorder has been found to run in families, which suggests that inheritance plays a strong role in determining who will get it.

Psychological factors, stressful life events, life transitions, and environment as well as often thinking in a way that exaggerates relatively normal bodily reactions are also believed to play a role in the onset of panic disorder. Often the first attacks are triggered by physical illnesses, major stress, or certain medications. People who tend to take on excessive responsibilities may develop a tendency to suffer panic attacks. Post-traumatic stress disorder (PTSD) patients also show a much higher rate of panic disorder than the general population.

Prepulse inhibition has been found to be reduced in patients with panic disorder.

Substance Misuse

Substance abuse is often correlated with panic attacks. In a study, 39% of people with panic disorder had abused substances. Of those who used alcohol, 63% reported that the alcohol use began prior to the onset of panic, and 59% of those abusing illicit drugs reported that drug use began first. The study that was conducted documented the panic-substance abuse relationship. Substance abuse began prior to the onset of panic and substances were used to self-medicate for panic attacks by only a few subjects.

In another study, 100 methamphetamine-dependent individuals were analysed for co-morbid psychiatric disorders; of the 100 individuals, 36% were categorised as having co-morbid psychiatric disorders. Mood and Psychotic disorders were more prevalent than anxiety disorders, which accounted for 7% of the 100 sampled individuals.

Smoking

Tobacco smoking increases the risk of developing panic disorder with or without agoraphobia and panic attacks; smoking started in adolescence or early adulthood particularly increases this risk of developing panic disorder. While the mechanism of how smoking increases panic attacks is not fully understood, a few hypotheses have been derived. Smoking cigarettes may lead to panic attacks by causing changes in respiratory function (e.g. feeling short of breath). These respiratory changes in turn can lead to the formation of panic attacks, as respiratory symptoms are a prominent feature of panic. Respiratory abnormalities have been found in children with high levels of anxiety, which suggests that a person with these difficulties may be susceptible to panic attacks, and thus more likely to subsequently develop panic disorder. Nicotine, a stimulant, could contribute to panic attacks. However, nicotine withdrawal may also cause significant anxiety which could contribute to panic attacks.

It is also possible that panic disorder patients smoke cigarettes as a form of self-medication to lessen anxiety. Nicotine and other psychoactive compounds with antidepressant properties in tobacco smoke which act as monoamine oxidase inhibitors in the brain can alter mood and have a calming effect, depending on dose.

Stimulants

A number of clinical studies have shown a positive association between caffeine ingestion and panic disorder and/or anxiogenic effects. People who have panic disorder are more sensitive to the anxiety-provoking effects of caffeine. One of the major anxiety-provoking effects of caffeine is an increase in heart rate.

Certain cold and flu medications containing decongestants may also contain pseudoephedrine, ephedrine, phenylephrine, naphazoline and oxymetazoline. These may be avoided by the use of decongestants formulated to prevent causing high blood pressure.

Alcohol and Sedatives

About 30% of people with panic disorder use alcohol and 17% use other psychoactive drugs. This is in comparison with 61% (alcohol) and 7.9% (other psychoactive drugs) of the general population who use alcohol and psychoactive drugs, respectively. Utilisation of recreational drugs or alcohol generally make symptoms worse. Most stimulant drugs (caffeine, nicotine, cocaine) would be expected to worsen the condition, since they directly increase the symptoms of panic, such as heart rate.

Deacon and Valentiner (2000) conducted a study that examined co-morbid panic attacks and substance use in a non-clinical sample of young adults who experienced regular panic attacks. The authors found that compared to healthy controls, sedative use was greater for non-clinical participants who experienced panic attacks. These findings are consistent with the suggestion made by Cox, Norton, Dorward, and Fergusson (1989) that panic disorder patients self-medicate if they believe that certain substances will be successful in alleviating their symptoms. If panic disorder patients are indeed self-medicating, there may be a portion of the population with undiagnosed panic disorder who will not seek professional help as a result of their own self-medication. In fact, for some patients panic disorder is only diagnosed after they seek treatment for their self-medication habit.

While alcohol initially helps ease panic disorder symptoms, medium- or long-term alcohol abuse can cause panic disorder to develop or worsen during alcohol intoxication, especially during alcohol withdrawal syndrome. This effect is not unique to alcohol but can also occur with long-term use of drugs which have a similar mechanism of action to alcohol such as the benzodiazepines which are sometimes prescribed as tranquilisers to people with alcohol problems. The reason chronic alcohol misuse worsens panic disorder is due to distortion of the brain chemistry and function.

Approximately 10% of patients will experience notable protracted withdrawal symptoms, which can include panic disorder, after discontinuation of benzodiazepines. Protracted withdrawal symptoms tend to resemble those seen during the first couple of months of withdrawal but usually are of a subacute level of severity compared to the symptoms seen during the first 2 or 3 months of withdrawal. It is not known definitively whether such symptoms persisting long after withdrawal are related to true pharmacological withdrawal or whether they are due to structural neuronal damage as a result of chronic use of benzodiazepines or withdrawal. Nevertheless, such symptoms do typically lessen as the months and years go by eventually disappearing altogether.

A significant proportion of patients attending mental health services for conditions including anxiety disorders such as panic disorder or social phobia have developed these conditions as a result of alcohol or sedative abuse. Anxiety may pre-exist alcohol or sedative dependence, which then acts to perpetuate or worsen the underlying anxiety disorder. Someone suffering the toxic effects of alcohol abuse or chronic sedative use or abuse will not benefit from other therapies or medications for underlying psychiatric conditions as they do not address the root cause of the symptoms. Recovery from sedative symptoms may temporarily worsen during alcohol withdrawal or benzodiazepine withdrawal.

Mechanism

The neuroanatomy of panic disorder largely overlaps with that of most anxiety disorders. Neuropsychological, neurosurgical, and neuroimaging studies implicate the insula, amygdala, hippocampus, anterior cingulate cortex (ACC), lateral prefrontal cortex, and periaqueductal grey. During acute panic attacks, viewing emotionally charged words, and rest, most studies find elevated blood flow or metabolism. However, the observation of amygdala hyperactivity is not entirely consistent, especially in studies that evoke panic attacks chemically. Hippocampus hyperactivity has been observed during rest and viewing emotionally charged pictures, which has been hypothesized to be related to memory retrieval bias towards anxious memories. Insula hyperactivity during the onset of and over the course of acute panic episodes is thought to be related to abnormal introceptive processes; the perception that bodily sensations are “wrong” is a transdiagnostic finding(i.e. found across multiple anxiety disorders), and may be related to insula dysfunction. Rodent and human studies heavily implicate the periaqueductal grey in generating fear responses, and abnormalities related to the structure and metabolism in the PAG have been reported in panic disorder. The frontal cortex is implicated in panic disorder by multiple lines of evidence. Damage to the dorsal ACC has been reported to lead to panic disorder. Elevated ventral ACC and dorsolateral prefrontal cortex during symptom provocation and viewing emotional stimuli have also been reported, although findings are not consistent.

Researchers studying some individuals with panic disorder propose they may have a chemical imbalance within the limbic system and one of its regulatory chemicals gamma-aminobutyric acid (GABA-A). The reduced production of GABA-A sends false information to the amygdala which regulates the body’s “fight or flight” response mechanism and, in return, produces the physiological symptoms that lead to the disorder. Clonazepam, an anticonvulsant benzodiazepine with a long half-life, has been successful in keeping the condition under control.

Recently, researchers have begun to identify mediators and moderators of aspects of panic disorder. One such mediator is the partial pressure of carbon dioxide, which mediates the relationship between panic disorder patients receiving breathing training and anxiety sensitivity; thus, breathing training affects the partial pressure of carbon dioxide in a patient’s arterial blood, which in turn lowers anxiety sensitivity. Another mediator is hypochondriacal concerns, which mediate the relationship between anxiety sensitivity and panic symptomatology; thus, anxiety sensitivity affects hypochondriacal concerns which, in turn, affect panic symptomatology.

Perceived threat control has been identified as a moderator within panic disorder, moderating the relationship between anxiety sensitivity and agoraphobia; thus, the level of perceived threat control dictates the degree to which anxiety sensitivity results in agoraphobia. Another recently identified moderator of panic disorder is genetic variations in the gene coding for galanin; these genetic variations moderate the relationship between females suffering from panic disorder and the level of severity of panic disorder symptomatology.

Diagnosis

The DSM-IV-TR diagnostic criteria for panic disorder require unexpected, recurrent panic attacks, followed in at least one instance by at least a month of a significant and related behaviour change, a persistent concern of more attacks, or a worry about the attack’s consequences. There are two types, one with and one without agoraphobia. Diagnosis is excluded by attacks due to a drug or medical condition, or by panic attacks that are better accounted for by other mental disorders.

The ICD-10 diagnostic criteria:

  • The essential feature is recurrent attacks of severe anxiety (panic), which are not restricted to any particular situation or set of circumstances and are therefore unpredictable.

The dominant symptoms include:

  • Sudden onset of palpitations.
  • Chest pain.
  • Choking sensations.
  • Dizziness.
  • Feelings of unreality (depersonalisation or derealisation).
  • Secondary fear of dying, losing control, or going mad.
  • Panic disorder should not be given as the main diagnosis if the person has a depressive disorder at the time the attacks start; in these circumstances, the panic attacks are probably secondary to depression.

The Panic Disorder Severity Scale (PDSS) is a questionnaire for measuring the severity of panic disorder.

Treatment

Panic disorder is a serious health problem that in many cases can be successfully treated, although there is no known cure. Identification of treatments that engender as full a response as possible, and can minimise relapse, is imperative. CBT and positive self-talk specific for panic are the treatments of choice for panic disorder. Several studies show that 85% to 90% of panic disorder patients treated with CBT recover completely from their panic attacks within 12 weeks. When CBT is not an option, pharmacotherapy can be used. SSRIs are considered a first-line pharmacotherapeutic option.

Psychotherapy

Panic disorder is not the same as phobic symptoms, although phobias commonly result from panic disorder. CBT and one tested form of psychodynamic psychotherapy have been shown efficacious in treating panic disorder with and without agoraphobia. A number of randomized clinical trials have shown that CBT achieves reported panic-free status in 70-90% of patients about 2 years after treatment.

A 2009 Cochrane review found little evidence concerning the efficacy of psychotherapy in combination with benzodiazepines such that recommendations could not be made.

Symptom inductions generally occur for one minute and may include:

  • Intentional hyperventilation creates lightheadedness, derealisation, blurred vision, and dizziness.
  • Spinning in a chair creates dizziness and disorientation.
  • Straw breathing creates dyspnoea and airway constriction.
  • Breath holding creates sensation of being out of breath.
  • Running in place creates increased heart rate, respiration, and perspiration.
  • Body tensing creates feelings of being tense and vigilant.

Another form of psychotherapy that has shown effectiveness in controlled clinical trials is panic-focused psychodynamic psychotherapy, which focuses on the role of dependency, separation anxiety, and anger in causing panic disorder. The underlying theory posits that due to biochemical vulnerability, traumatic early experiences, or both, people with panic disorder have a fearful dependence on others for their sense of security, which leads to separation anxiety and defensive anger. Therapy involves first exploring the stressors that lead to panic episodes, then probing the psychodynamics of the conflicts underlying panic disorder and the defence mechanisms that contribute to the attacks, with attention to transference and separation anxiety issues implicated in the therapist-patient relationship.

Comparative clinical studies suggest that muscle relaxation techniques and breathing exercises are not efficacious in reducing panic attacks. In fact, breathing exercises may actually increase the risk of relapse.

Appropriate treatment by an experienced professional can prevent panic attacks or at least substantially reduce their severity and frequency – bringing significant relief to 70% to 90% of people with panic disorder. Relapses may occur, but they can often be effectively treated just like the initial episode.

vanApeldoorn, F.J. et al. (2011) demonstrated the additive value of a combined treatment incorporating an SSRI treatment intervention with CBT. Gloster et al. (2011) went on to examine the role of the therapist in CBT. They randomised patients into two groups: one being treated with CBT in a therapist guided environment, and the second receiving CBT through instruction only, with no therapist guided sessions. The findings indicated that the first group had a somewhat better response rate, but that both groups demonstrated a significant improvement in reduction of panic symptomatology. These findings lend credibility to the application of CBT programs to patients who are unable to access therapeutic services due to financial, or geographic inaccessibility. Koszycky et al. (2011) discuss the efficacy of self-administered CBT (SCBT) in situations where patients are unable to retain the services of a therapist. Their study demonstrates that it is possible for SCBT in combination with an SSRI to be as effective as therapist-guided CBT with SSRI. Each of these studies contributes to a new avenue of research that allows effective treatment interventions to be made more easily accessible to the population.

Cognitive Behavioural Therapy (CBT)

CBT encourages patients to confront the triggers that induce their anxiety. By facing the very cause of the anxiety, it is thought to help diminish the irrational fears that are causing the issues to begin with. The therapy begins with calming breathing exercises, followed by noting the changes in physical sensations felt as soon as anxiety begins to enter the body. Many clients are encouraged to keep journals. In other cases, therapists may try and induce feelings of anxiety so that the root of the fear can be identified.

Comorbid clinical depression, personality disorders and alcohol abuse are known risk factors for treatment failure.

As with many disorders, having a support structure of family and friends who understand the condition can help increase the rate of recovery. During an attack, it is not uncommon for the sufferer to develop irrational, immediate fear, which can often be dispelled by a supporter who is familiar with the condition. For more serious or active treatment, there are support groups for anxiety sufferers which can help people understand and deal with the disorder.

Current treatment guidelines American Psychiatric Association and the American Medical Association primarily recommend either CBT or one of a variety of psychopharmacological interventions. Some evidence exists supporting the superiority of combined treatment approaches.

Another option is self-help based on principles of CBT. Using a book or a website, a person does the kinds of exercises that would be used in therapy, but they do it on their own, perhaps with some email or phone support from a therapist. A systematic analysis of trials testing this kind of self-help found that websites, books, and other materials based on CBT could help some people. The best-studied conditions are panic disorder and social phobia.

Interoceptive Techniques

Interoceptive exposure is sometimes used for panic disorder. People’s interoceptive triggers of anxiety are evaluated one-by-one before conducting interoceptive exposures, such as addressing palpitation sensitivity via light exercise. Despite evidence of its clinical efficacy, this practice is reportedly used by only 12-20% of psychotherapists. Potential reasons for this underutilisation include “lack of training sites, logistical hurdles (e.g. occasional need for exposure durations longer than a standard therapy session), policies against conducting exposures outside of the workplace setting, and perhaps most tellingly, negative therapist beliefs (e.g. that interoceptive exposures are unethical, intolerable, or even harmful).”

Medication

Appropriate medications are effective for panic disorder. Selective serotonin reuptake inhibitors are first line treatments rather than benzodiazepines due to concerns with the latter regarding tolerance, dependence and abuse. Although there is little evidence that pharmacological interventions can directly alter phobias, few studies have been performed, and medication treatment of panic makes phobia treatment far easier (an example in Europe where only 8% of patients receive appropriate treatment).

Medications can include:

  • Antidepressants (SSRIs, MAOIs, tricyclic antidepressants and norepinephrine reuptake inhibitors).
  • Antianxiety agents (benzodiazepines):
    • Use of benzodiazepines for panic disorder is controversial.
    • The American Psychiatric Association states that benzodiazepines can be effective for the treatment of panic disorder and recommends that the choice of whether to use benzodiazepines, antidepressants with anti-panic properties or psychotherapy should be based on the individual patient’s history and characteristics.
    • Other experts believe that benzodiazepines are best avoided due to the risks of the development of tolerance and physical dependence.
    • The World Federation of Societies of Biological Psychiatry, say that benzodiazepines should not be used as a first-line treatment option but are an option for treatment-resistant cases of panic disorder.
    • Despite increasing focus on the use of antidepressants and other agents for the treatment of anxiety as recommended best practice, benzodiazepines have remained a commonly used medication for panic disorder.
    • They reported that in their view there is insufficient evidence to recommend one treatment over another for panic disorder.
    • The APA noted that while benzodiazepines have the advantage of a rapid onset of action, that this is offset by the risk of developing a benzodiazepine dependence.
    • The UKs National Institute of Clinical Excellence (NICE) came to a different conclusion, they pointed out the problems of using uncontrolled clinical trials to assess the effectiveness of pharmacotherapy and based on placebo-controlled research they concluded that benzodiazepines were not effective in the long-term for panic disorder and recommended that benzodiazepines not be used for longer than 4 weeks for panic disorder.
    • Instead NICE clinical guidelines recommend alternative pharmacotherapeutic or psychotherapeutic interventions.
    • When compared to placebos, benzodiazepines demonstrate possible superiority in the short term but the evidence is low quality with limited applicability to clinical practice.

Other Treatments

For some people, anxiety can be greatly reduced by discontinuing the use of caffeine. Anxiety can temporarily increase during caffeine withdrawal.

Epidemiology

Panic disorder typically begins during early adulthood; roughly half of all people who have panic disorder develop the condition between the ages of 17 and 24, especially those subjected to traumatic experiences. However, some studies suggest that the majority of young people affected for the first time are between the ages of 25 and 30. Women are twice as likely as men to develop panic disorder and it occurs far more often in people with above average intelligence.

Panic disorder can continue for months or years, depending on how and when treatment is sought. If left untreated, it may worsen to the point where one’s life is seriously affected by panic attacks and by attempts to avoid or conceal the condition. In fact, many people have had problems with personal relationships, education and employment while struggling to cope with panic disorder. Some people with panic disorder may conceal their condition because of the stigma of mental illness. In some individuals, symptoms may occur frequently for a period of months or years, then many years may pass with little or no symptoms. In some cases, the symptoms persist at the same level indefinitely. There is also some evidence that many individuals (especially those who develop symptoms at an early age) may experience symptom cessation later in life (e.g. past age 50).

In 2000, the World Health Organisation found prevalence and incidence rates for panic disorder to be very similar across the globe. Age-standardised prevalence per 100,000 ranged from 309 in Africa to 330 in East Asia for men and from 613 in Africa to 649 in North America, Oceania, and Europe for women.

Children

A retrospective study has shown that 40% of adult panic disorder patients reported that their disorder began before the age of 20. In an article examining the phenomenon of panic disorder in youth, Diler et al. (2004) found that only a few past studies have examined the occurrence of juvenile panic disorder. They report that these studies have found that the symptoms of juvenile panic disorder almost replicate those found in adults (e.g. heart palpitations, sweating, trembling, hot flashes, nausea, abdominal distress, and chills). The anxiety disorders co-exist with staggeringly high numbers of other mental disorders in adults. The same comorbid disorders that are seen in adults are also reported in children with juvenile panic disorder. Last and Strauss (1989) examined a sample of 17 adolescents with panic disorder and found high rates of comorbid anxiety disorders, major depressive disorder, and conduct disorders. Eassau et al. (1999) also found a high number of comorbid disorders in a community-based sample of adolescents with panic attacks or juvenile panic disorder. Within the sample, adolescents were found to have the following comorbid disorders: major depressive disorder (80%), dysthymic disorder (40%), generalised anxiety disorder (40%), somatoform disorders (40%), substance abuse (40%), and specific phobia (20%). Consistent with this previous work, Diler et al. (2004) found similar results in their study in which 42 youths with juvenile panic disorder were examined. Compared to non-panic anxiety disordered youths, children with panic disorder had higher rates of comorbid major depressive disorder and bipolar disorder.

Children differ from adolescents and adults in their interpretation and ability to express their experience. Like adults, children experience physical symptoms including accelerated heart rate, sweating, trembling or shaking, shortness of breath, nausea or stomach pain, dizziness or light-headedness. In addition, children also experience cognitive symptoms like fear of dying, feelings of being detached from oneself, feelings of losing control or going crazy, but they are unable to vocalize these higher-order manifestations of fear. They simply know that something is going wrong and that they are very afraid. Children can only describe physical symptoms. They have not yet developed the constructs to put these symptoms together and label them as fear. Parents often feel helpless when they watch a child suffer. They can help children give a name to their experience, and empower them to overcome the fear they are experiencing.

The role of the parent in treatment and intervention for children diagnosed with panic disorder is discussed by McKay & Starch (2011). They point out that there are several levels at which parental involvement should be considered. The first involves the initial assessment. Parents, as well as the child, should be screened for attitudes and treatment goals, as well as for levels of anxiety or conflict in the home. The second involves the treatment process in which the therapist should meet with the family as a unit as frequently as possible. Ideally, all family members should be aware and trained in the process of CBT in order to encourage the child to rationalize and face fears rather than employ avoidant safety behaviours. McKay & Storch (2011) suggest training/modelling of therapeutic techniques and in-session involvement of the parents in the treatment of children to enhance treatment efficacy.

Despite the evidence pointing to the existence of early-onset panic disorder, the DSM-IV-TR currently only recognizes six anxiety disorders in children: separation anxiety disorder, generalised anxiety disorder, specific phobia, obsessive-compulsive disorder, social anxiety disorder (a.k.a. social phobia), and post-traumatic stress disorder. Panic disorder is notably excluded from this list.

What is a Panic Attack?

Introduction

Panic attacks are sudden periods of intense fear that may include palpitations, sweating, shaking, shortness of breath, numbness, or a feeling of impending doom. The maximum degree of symptoms occurs within minutes. Typically they last for about 30 minutes but the duration can vary from seconds to hours. There may be a fear of losing control or chest pain. Panic attacks themselves are not dangerous physically.

Panic attacks can occur due to several disorders including panic disorder, social anxiety disorder, post-traumatic stress disorder, drug use disorder, depression, and medical problems. They can either be triggered or occur unexpectedly. Smoking, caffeine, and psychological stress increase the risk of having a panic attack. Before diagnosis, conditions that produce similar symptoms should be ruled out, such as hyperthyroidism, hyperparathyroidism, heart disease, lung disease, drug use, and dysautonomia.

Treatment of panic attacks should be directed at the underlying cause. In those with frequent attacks, counselling or medications may be used. Breathing training and muscle relaxation techniques may also help. Those affected are at a higher risk of suicide.

In Europe, about 3% of the population has a panic attack in a given year while in the United States they affect about 11%. They are more common in females than in males. They often begin during puberty or early adulthood. Children and older people are less commonly affected.

Signs and Symptoms

People with panic attacks often report a fear of dying or heart attack, flashing vision, faintness or nausea, numbness throughout the body, heavy breathing and hyperventilation, or loss of body control. Some people also suffer from tunnel vision, mostly due to blood flow leaving the head to more critical parts of the body in defence. These feelings may provoke a strong urge to escape or flee the place where the attack began (a consequence of the “fight-or-flight response”, in which the hormone causing this response is released in significant amounts). This response floods the body with hormones, particularly epinephrine (adrenaline), which aid it in defending against harm.

A panic attack can result when up-regulation by the sympathetic nervous system (SNS) is not moderated by the parasympathetic nervous system (PNS). The most common symptoms include trembling, dyspnoea (shortness of breath), heart palpitations, chest pain (or chest tightness), hot flashes, cold flashes, burning sensations (particularly in the facial or neck area), sweating, nausea, dizziness (or slight vertigo), light-headedness, heavy-headedness, hyperventilation, paraesthesia’s’ (tingling sensations), sensations of choking or smothering, difficulty moving, depersonalisation and/or derealization. These physical symptoms are interpreted with alarm in people prone to panic attacks. This results in increased anxiety and forms a positive feedback loop.

Shortness of breath and chest pain are the predominant symptoms. People experiencing a panic attack may incorrectly attribute them to a heart attack and thus seek treatment in an emergency room. Because chest pain and shortness of breath are hallmark symptoms of cardiovascular illnesses, including unstable angina and myocardial infarction (heart attack), a diagnosis of exclusion (ruling out other conditions) must be performed before diagnosing a panic attack. It is especially important to do this for people whose mental health and heart health statuses are unknown. This can be done using an electrocardiogram and mental health assessments.

Panic attacks are distinguished from other forms of anxiety by their intensity and their sudden, episodic nature. They are often experienced in conjunction with anxiety disorders and other psychological conditions, although panic attacks are not generally indicative of a mental disorder.

Causes

There are long-term, biological, environmental, and social causes of panic attacks. In 1993, Fava et al. proposed a staging method of understanding the origins of disorders. The first stage in developing a disorder involves predisposing factors, such as genetics, personality, and a lack of well-being. Panic disorder often occurs in early adulthood, although it may appear at any age. It occurs more frequently in women and more often in people with above-average intelligence. Various twin studies where one identical twin has an anxiety disorder have reported a high incidence of the other twin also having an anxiety disorder diagnosis.

Biological causes may include obsessive-compulsive disorder, postural orthostatic tachycardia syndrome, post-traumatic stress disorder, hypoglycaemia, hyperthyroidism, Wilson’s disease, mitral valve prolapse, pheochromocytoma, and inner ear disturbances (labyrinthitis). Dysregulation of the norepinephrine system in the locus coeruleus, an area of the brain stem, has been linked to panic attacks.

Panic attacks may also occur due to short-term stressors. Significant personal loss, including an emotional attachment to a romantic partner, life transitions, and significant life changes may all trigger a panic attack to occur. A person with an anxious temperament, excessive need for reassurance, hypochondriacal fears, overcautious view of the world, and cumulative stress have been correlated with panic attacks. In adolescents, social transitions may also be a cause.

People will often experience panic attacks as a direct result of exposure to an object/situation that they have a phobia for. Panic attacks may also become situationally-bound when certain situations are associated with panic due to previously experiencing an attack in that particular situation. People may also have a cognitive or behavioural predisposition to having panic attacks in certain situations.

Some maintaining causes include avoidance of panic-provoking situations or environments, anxious/negative self-talk (“what-if” thinking), mistaken beliefs (“these symptoms are harmful and/or dangerous”), and withheld feelings.

Hyperventilation syndrome may occur when a person breathes from the chest, which can lead to over-breathing (exhaling excessive carbon dioxide related to the amount of oxygen in one’s bloodstream). Hyperventilation syndrome can cause respiratory alkalosis and hypocapnia. This syndrome often involves prominent mouth breathing as well. This causes a cluster of symptoms, including rapid heartbeat, dizziness, and lightheadedness, which can trigger panic attacks.

Panic attacks may also be caused by substances. Discontinuation or marked reduction in the dose of a substance such as a drug (drug withdrawal), for example, an antidepressant (antidepressant discontinuation syndrome), can cause a panic attack. According to the Harvard Mental Health Letter, “the most commonly reported side effects of smoking marijuana are anxiety and panic attacks. Studies report that about 20% to 30% of recreational users experience such problems after smoking marijuana.” Cigarette smoking is another substance that has been linked to panic attacks.

A common denominator of current psychiatric approaches to panic disorder is that no real danger exists, and the person’s anxiety is inappropriate.

Panic Disorder

Refer to Panic Disorder.

People who have repeated, persistent attacks or feel severe anxiety about having another attack are said to have panic disorder. Panic disorder is strikingly different from other types of anxiety disorders in that panic attacks are often sudden and unprovoked. However, panic attacks experienced by those with panic disorder may also be linked to or heightened by certain places or situations, making daily life difficult.

Agoraphobia

Refer to Agoraphobia and Hikikomori.

Agoraphobia is an anxiety disorder that primarily consists of the fear of experiencing a difficult or embarrassing situation from which the sufferer cannot escape. Panic attacks are commonly linked to agoraphobia and the fear of not being able to escape a bad situation. As the result, severe sufferers of agoraphobia may become confined to their homes, experiencing difficulty traveling from this “safe place”. The word “agoraphobia” is an English adoption of the Greek words agora (αγορά) and Phobos (φόβος). The term “agora” refers to the place where ancient Greeks used to gather and talk about issues of the city, so it applies to any or all public places; however, the essence of agoraphobia is a fear of panic attacks especially if they occur in public as the victim may feel like he or she has no escape. In the case of agoraphobia caused by a social phobia or social anxiety, sufferers may be very embarrassed by having a panic attack publicly in the first place. This translation is the reason for the common misconception that agoraphobia is a fear of open spaces, and is not clinically accurate. Agoraphobia, as described in this manner, is a symptom professionals check for when making a diagnosis of panic disorder. In Japan, people who exhibit extreme agoraphobia to the point of becoming unwilling or unable to leave their homes are referred to as Hikikomori. The phenomena in general is known by the same name, and it is estimated that roughly half a million Japanese youths are Hikikomori.

People who have had a panic attack in certain situations may develop irrational fears, called phobias, of these situations and begin to avoid them. Eventually, the pattern of avoidance and level of anxiety about another attack may reach the point where individuals with panic disorder are unable to drive or even step out of the house. At this stage, the person is said to have panic disorder with agoraphobia.

Experimentally Induced

Panic attack symptoms can be experimentally induced in the laboratory by various means. Among them, for research purposes, by administering a bolus injection of the neuropeptide cholecystokinin-tetrapeptide (CCK-4). Various animal models of panic attacks have been experimentally studied.

Neurotransmitter Imbalances

Many neurotransmitters are affected when the body is under the increased stress and anxiety that accompany a panic attack. Some include serotonin, GABA (gamma-aminobutyric acid), dopamine, norepinephrine, and glutamate. More research into how these neurotransmitters interact with one another during a panic attack is needed to make any solid conclusions, however.

An increase of serotonin in certain pathways of the brain seems to be correlated with reduced anxiety. More evidence that suggests serotonin plays a role in anxiety is that people who take SSRIs tend to feel a reduction of anxiety when their brain has more serotonin available to use.

The main inhibitory neurotransmitter in the central nervous system (CNS) is GABA. Most of the pathways that use GABA tend to reduce anxiety immediately.

Dopamine’s role in anxiety is not well understood. Some antipsychotic medications that affect dopamine production have been proven to treat anxiety. However, this may be attributed to dopamine’s tendency to increase feelings of self-efficacy and confidence, which indirectly reduces anxiety.

Many physical symptoms of anxiety, such as rapid heart rate and hand tremors, are regulated by norepinephrine. Drugs that counteract norepinephrine’s effect may be effective in reducing the physical symptoms of a panic attack. Nevertheless, some drugs that increase ‘background’ norepinephrine levels such as tricyclics and SNRIs are effective for the long-term treatment of panic attacks, possibly by blunting the norepinephrine spikes associated with panic attacks.

Because glutamate is the primary excitatory neurotransmitter involved in the central nervous system (CNS), it can be found in almost every neural pathway in the body. Glutamate is likely involved in conditioning, which is the process by which certain fears are formed, and extinction, which is the elimination of those fears.

Pathophysiology

The symptoms of a panic attack may cause the person to feel that their body is failing. The symptoms can be understood as follows. First, there is frequently the sudden onset of fear with little provoking stimulus. This leads to a release of adrenaline (epinephrine) which brings about the fight-or-flight response when the body prepares for strenuous physical activity. This leads to an increased heart rate (tachycardia), rapid breathing (hyperventilation) which may be perceived as shortness of breath (dyspnoea), and sweating. Because strenuous activity rarely ensues, the hyperventilation leads to a drop in carbon dioxide levels in the lungs and then in the blood. This leads to shifts in blood pH (respiratory alkalosis or hypocapnia), causing compensatory metabolic acidosis activating chemosensing mechanisms that translate this pH shift into autonomic and respiratory responses.

Moreover, this hypocapnia and release of adrenaline during a panic attack cause vasoconstriction resulting in slightly less blood flow to the head which causes dizziness and lightheadedness. A panic attack can cause blood sugar to be drawn away from the brain and toward the major muscles. Neuroimaging suggests heightened activity in the amygdala, thalamus, hypothalamus, and brainstem regions including the periaqueductal gray, parabrachial nucleus, and Locus coeruleus. In particular, the amygdala has been suggested to have a critical role. The combination of increased activity in the amygdala (fear centre) and brainstem along with decreased blood flow and blood sugar in the brain can lead to decreased activity in the prefrontal cortex (PFC) region of the brain. There is evidence that having an anxiety disorder increases the risk of cardiovascular disease (CVD). Those affected also have a reduction in heart rate variability.

Cardiovascular Disease

People who have been diagnosed with panic disorder have approximately double the risk of coronary heart disease. Certain stress responses to depression also have been shown to increase the risk and those diagnosed with both depression and panic disorder are nearly three times more at risk.

Diagnosis

DSM-5 diagnostic criteria for a panic attack include a discrete period of intense fear or discomfort, in which four (or more) of the following symptoms developed abruptly and reached a peak within minutes:

  • Palpitations, and/or accelerated heart rate.
  • Sweating.
  • Trembling or shaking.
  • Sensations of shortness of breath or being smothered.
  • Feeling of choking.
  • Chest pain or discomfort.
  • Nausea or abdominal distress.
  • Feeling dizzy, unsteady, lightheaded, or faint.
  • Derealization (feelings of unreality) or depersonalisation (being detached from oneself).
  • Fear of losing control or going insane.
  • Sense of impending doom.
  • Paraesthesia’s (numbness or tingling sensations).
  • Chills or hot flashes..

In DSM-5, culture-specific symptoms (e.g., tinnitus, neck soreness, headache, and uncontrollable screaming or crying) may be seen. Such symptoms should not count as one of the four required symptoms.

Some or all of these symptoms can be found in the presence of a pheochromocytoma.

Screening tools such as the Panic Disorder Severity Scale can be used to detect possible cases of disorder and suggest the need for a formal diagnostic assessment.

Treatment

Panic disorder can be effectively treated with a variety of interventions, including psychological therapies and medication. Cognitive-behavioural therapy (CBT) has the most complete and longest duration of effect, followed by specific selective serotonin reuptake inhibitors (SSRIs). A 2009 review found positive results from therapy and medication and a much better result when the two were combined.

Lifestyle Changes

Caffeine may cause or exacerbate panic anxiety. Anxiety can temporarily increase during withdrawal from caffeine and various other drugs.

Increased and regimented aerobic exercise such as running has been shown to have a positive effect on combating panic anxiety. There is evidence that suggests that this effect is correlated to the release of exercise-induced endorphins and the subsequent reduction of the stress hormone cortisol.

There remains a chance of panic symptoms becoming triggered or being made worse due to increased respiration rate that occurs during aerobic exercise. This increased respiration rate can lead to hyperventilation and hyperventilation syndrome, which mimics symptoms of a heart attack, thus inducing a panic attack. The benefits of incorporating an exercise regimen have shown the best results when paced accordingly.

Muscle relaxation techniques are useful to some individuals. These can be learned using recordings, videos, or books. While muscle relaxation has proved to be less effective than CBT in controlled trials, many people still find at least temporary relief from muscle relaxation.

Breathing Exercises

In the great majority of cases, hyperventilation is involved, exacerbating the effects of the panic attack. Breathing retraining exercise helps to rebalance the oxygen and CO2 levels in the blood.

David D. Burns recommends breathing exercises for those suffering from anxiety. One such breathing exercise is a 5-2-5 count. Using the stomach (or diaphragm) – and not the chest – inhale (feel the stomach come out, as opposed to the chest expanding) for 5 seconds. As the maximal point at inhalation is reached, hold the breath for 2 seconds. Then slowly exhale, over 5 seconds. Repeat this cycle twice and then breathe ‘normally’ for 5 cycles (1 cycle = 1 inhale + 1 exhale). The point is to focus on breathing and relax the heart rate. Regular diaphragmatic breathing may be achieved by extending the out-breath by counting or humming.

Although breathing into a paper bag was a common recommendation for short-term treatment of symptoms of an acute panic attack, it has been criticised as inferior to measured breathing, potentially worsening the panic attack and possibly reducing needed blood oxygen. While the paper bag technique increases needed carbon dioxide and so reduces symptoms, it may excessively lower oxygen levels in the bloodstream.

Capnometry, which provides exhaled CO2 levels, may help guide breathing.

Therapy

According to the American Psychological Association, “most specialists agree that a combination of cognitive and behavioural therapies are the best treatment for panic disorder. Medication might also be appropriate in some cases.” The first part of therapy is largely informational; many people are greatly helped by simply understanding exactly what panic disorder is and how many others suffer from it. Many people who suffer from panic disorder are worried that their panic attacks mean they are “going crazy” or that the panic might induce a heart attack. Cognitive restructuring helps people replace those thoughts with more realistic, positive ways of viewing the attacks. Avoidance behaviour is one of the key aspects that prevent people with frequent panic attacks from functioning healthily. Exposure therapy, which includes repeated and prolonged confrontation with feared situations and body sensations, helps weaken anxiety responses to these external and internal stimuli and reinforce realistic ways of viewing panic symptoms.

In deeper level psychoanalytic approaches, in particular object relations theory, panic attacks are frequently associated with splitting (psychology), paranoid-schizoid and depressive positions, and paranoid anxiety. They are often found comorbid with borderline personality disorder and child sexual abuse. Paranoid anxiety may reach the level of a persecutory anxiety state.

Meditation may also be helpful in the treatment of panic disorders. There was a meta-analysis of the comorbidity of panic disorders and agoraphobia. It used exposure therapy to treat patients over a period. Hundreds of patients were used in these studies and they all met the DSM-IV criteria for both of these disorders. A result was that 32% of patients had a panic episode after treatment. They concluded that the use of exposure therapy has lasting efficacy for a client who is living with a panic disorder and agoraphobia.

The efficacy of group therapy treatment over conventional individual therapy for people with panic disorder with or without agoraphobia appears similar.

Medication

Medication options for panic attacks typically include benzodiazepines and antidepressants. Benzodiazepines are being prescribed less often because of their potential side effects, such as dependence, fatigue, slurred speech, and memory loss. Antidepressant treatments for panic attacks include selective serotonin reuptake inhibitors (SSRIs), serotonin noradrenaline reuptake inhibitors (SNRIs), tricyclic antidepressants (TCAs), and MAO inhibitors (MAOIs). SSRIs in particular tend to be the first drug treatment used to treat panic attacks. Selective serotonin reuptake inhibitors (SSRIs) and tricyclic antidepressants appear similar for short-term efficacy.

SSRIs carry a relatively low risk since they are not associated with much tolerance or dependence, and are difficult to overdose with. TCAs are similar to SSRIs in their many advantages but come with more common side effects such as weight gain and cognitive disturbances. They are also easier to overdose on. MAOIs are generally suggested for patients who have not responded to other forms of treatment.

While the use of drugs in treating panic attacks can be very successful, it is generally recommended that people also be in some form of therapy, such as CBT. Drug treatments are usually used throughout the duration of panic attack symptoms and discontinued after the patient has been free of symptoms for at least six months. It is usually safest to withdraw from these drugs gradually while undergoing therapy. While drug treatment seems promising for children and adolescents, they are at an increased risk of suicide while taking these medications and their well-being should be monitored closely.

Prognosis

Roughly one-third are treatment-resistant. These people continue to have panic attacks and various other panic disorder symptoms after receiving treatment.

Many people being treated for panic attacks begin to experience limited symptom attacks. These panic attacks are less comprehensive, with fewer than four bodily symptoms being experienced.

It is not unusual to experience only one or two symptoms at a time, such as vibrations in their legs, shortness of breath, or an intense wave of heat traveling up their bodies, which is not similar to hot flashes due to oestrogen shortage. Some symptoms, such as vibrations in the legs, are sufficiently different from any normal sensation that they indicate a panic disorder. Other symptoms on the list can occur in people who may or may not have panic disorder. Panic disorder does not require four or more symptoms to all be present at the same time. Causeless panic and racing heartbeat are sufficient to indicate a panic attack.

Epidemiology

In Europe, about 3% of the population has a panic attack in a given year while in the United States they affect about 11%. They are more common in females than in males. They often begin during puberty or early adulthood. Children and older people are less commonly affected. A meta-analysis was conducted on data collected about twin studies and family studies on the link between genes and panic disorder. The researchers also examined the possibility of a link to phobias, obsessive-compulsive disorder (OCD), and generalised anxiety disorder. The researchers used a database called MEDLINE to accumulate their data. The results concluded that the aforementioned disorders have a genetic component and are inherited or passed down through genes. For the non-phobias, the likelihood of inheriting is 30-40%, and for the phobias, it was 50-60%.

Mental Health in Japan: The Rise of Recluses

Did you know that the pressures from work and society are causing more people in Japan to shun the outside world.

In the attached article by The Economist we can read about “Mika Shibata’s youngest son”, aged 26, who has not emerged from his bedroom for a year! (The Economist, 2019, p.49).

In an article by Andrew McKirdy, for the JapanTimes.co.jp, he states that a Government survey suggested that 613,000 people, between the ages of 40 and 64, are believed to be hikikomori.

This is up from the estimated 541,000 people aged between 15 and 39 that a 2015 Cabinet Office survey found to be hikikomori.

References

McKirdy, A. (2019) The prison inside: Japan’s hikikomori lack relationships, not physical spaces. Available from World Wide Web: https://www.japantimes.co.jp/life/2019/06/01/lifestyle/prison-inside-japans-hikikomori-lack-relationships-not-physical-spaces/#.Xil8ymieSUk. [Accessed: 23 January, 2020].

The Economist. (2019) Mental Health in Japan: The Rise of Recluses. The Economist. 30 November 2019.