Bicameral mentality

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https://en.wikipedia.org/wiki/Bicameral_mentality 

Bicameral mentality is a hypothesis introduced by Julian Jaynes who argued human ancestors as late as the Ancient Greeks did not consider emotions and desires as stemming from their own minds but as the consequences of actions of gods external to themselves. The theory posits that the human mind once operated in a state in which cognitive functions were divided between one part of the brain which appears to be "speaking", and a second part which listens and obeys—a bicameral mind, and that the breakdown of this division gave rise to consciousness in humans. The term was coined by Jaynes who presented the idea in his 1976 book The Origin of Consciousness in the Breakdown of the Bicameral Mind, wherein he made the case that a bicameral mentality was the normal and ubiquitous state of the human mind as recently as 3,000 years ago, near the end of the Mediterranean bronze age.

The Origin of Consciousness

Main article: The Origin of Consciousness in the Breakdown of the Bicameral Mind

Jaynes uses "bicameral" (two chambers) to describe a mental state in which the experiences and memories of the right hemisphere of the brain are transmitted to the left hemisphere via auditory hallucinations. The metaphor is based on the idea of lateralization of brain function although each half of a normal human brain is constantly communicating with the other through the corpus callosum. The metaphor is not meant to imply that the two halves of the bicameral brain were "cut off" from each other but that the bicameral mind was experienced as a different, non-conscious mental schema wherein volition in the face of novel stimuli was mediated through a linguistic control mechanism and experienced as auditory verbal hallucination.

Definition

Bicameral mentality is non-conscious in its inability to reason and articulate about mental contents through meta-reflection, reacting without explicitly realizing and without the meta-reflective ability to give an account of why one did so. The bicameral mind thus lacks metaconsciousness, autobiographical memory, and the capacity for executive "ego functions" such as deliberate mind-wandering and conscious introspection of mental content. When bicameral mentality as a method of social control was no longer adaptive in complex civilizations, this mental model was replaced by the conscious mode of thought which, Jaynes argued, is grounded in the acquisition of metaphorical language learned by exposure to narrative practice.

According to Jaynes, ancient people in the bicameral state of mind experienced the world in a manner that has some similarities to that of a person with schizophrenia. Rather than making conscious evaluations in novel or unexpected situations, the person hallucinated a voice or "god" giving admonitory advice or commands and obey without question: One was not at all conscious of one's own thought processes per se. Jaynes's hypothesis is offered as a possible explanation of "command hallucinations" that often direct the behavior of those with first rank symptoms of schizophrenia, as well as other voice hearers.

Jaynes's evidence

Jaynes built a case for this hypothesis that human brains existed in a bicameral state until as recently as 3,000 years ago by citing evidence from many diverse sources including historical literature. He took an interdisciplinary approach, drawing data from many different fields. Jaynes asserted that, until roughly the times written about in Homer's Iliad, humans did not generally have the self-awareness characteristic of consciousness as most people experience it today. Rather, the bicameral individual was guided by mental commands believed to be issued by external "gods"—commands which were recorded in ancient myths, legends and historical accounts. This is exemplified not only in the commands given to characters in ancient epics but also the very muses of Greek mythology which "sang" the poems. According to Jaynes, the ancients literally heard muses as the direct source of their music and poetry.

Jaynes asserts that in the Iliad and sections of the Old Testament no mention is made of any kind of cognitive processes such as introspection, and there is no apparent indication that the writers were self-aware. Jaynes suggests, the older portions of the Old Testament (such as the Book of Amos) have few or none of the features of some later books of the Old Testament (such as Ecclesiastes) as well as later works such as Homer's Odyssey, which show indications of a profoundly different kind of mentality—an early form of consciousness.

In ancient times, Jaynes noted, gods were generally much more numerous and much more anthropomorphic than in modern times, and speculates that this was because each bicameral person had their own "god" who reflected their own desires and experiences.

He also noted that in ancient societies the corpses of the dead were often treated as though still alive (being seated, dressed, and even fed) as a form of ancestor worship, and Jaynes argued that the dead bodies were presumed to be still living and the source of auditory hallucinations. This adaptation to the village communities of 100 individuals or more formed the core of religion.

Jaynes inferred that these "voices" came from the right brain counterparts of the left brain language centres; specifically, the counterparts to Wernicke's area and Broca's area. These regions are somewhat dormant in the right brains of most modern humans, but Jaynes noted that some studies show that auditory hallucinations correspond to increased activity in these areas of the brain.

Jaynes notes that even at the time of publication there is no consensus as to the cause or origins of schizophrenia. Jaynes argues that schizophrenia is a vestige of humanity's earlier bicameral state. Recent evidence shows that many people with schizophrenia do not just hear random voices but experience "command hallucinations" instructing their behavior or urging them to commit certain acts, such as walking into the ocean, which the listener feels they have no choice but to follow. Jaynes also argues people with schizophrenia feel a loss of identity due to hallucinated voices taking the place of their internal monologue.

As support for Jaynes's argument, these command hallucinations are little different from the commands from gods which feature prominently in ancient stories. Indirect evidence supporting Jaynes's theory that hallucinations once played an important role in human mentality can be found in the 2012 book Muses, Madmen, and Prophets: Rethinking the History, Science, and Meaning of Auditory Hallucination by Daniel Smith.

Breakdown

Jaynes theorized that a shift from bicameral mentality marked the beginning of introspection and consciousness as we know it today. According to Jaynes, this bicameral mentality began malfunctioning or "breaking down" during the 2nd millennium BCE. He speculates that primitive ancient societies tended to collapse periodically: for example, Egypt's Intermediate Periods, as well as the periodically vanishing cities of the Mayas, as changes in the environment strained the socio-cultural equilibria sustained by this bicameral mindset.

The Bronze age collapse of the 2nd millennium BCE led to mass migrations and created a rash of unexpected situations and stresses which required ancient minds to become more flexible and creative. Self-awareness, or consciousness, was the culturally evolved solution to this problem. This necessity of communicating commonly observed phenomena among individuals who shared no common language or cultural upbringing encouraged those communities to become self-aware to survive in a new environment. Thus consciousness, like bicameral mentality, emerged as a neurological adaptation to social complexity in a changing world.

Jaynes further argues that divination, prayer, and oracles arose during this breakdown period, in an attempt to summon instructions from the "gods" whose voices could no longer be heard. The consultation of special bicamerally operative individuals, or of divination by casting lots and so forth, was a response to this loss, a transitional era depicted, for example, in the book of 1 Samuel. It was also evidenced in children who could communicate with the gods, but as their neurology was set by language and society they gradually lost that ability. Those who continued prophesying, being bicameral according to Jaynes, could be killed.

Leftovers of the bicameral mind today, according to Jaynes, include mental illnesses such as schizophrenia. Jaynes says that there is no evidence of insanity existing prior to the breakdown of the bicameral mind and that this is indirect evidence for his theory. He considered that previous claims of insanity in Homeric literature are based on mistranslations.

Reception

Popular reception

An early (1977) reviewer considered Jaynes's hypothesis worthy and offered conditional support, arguing the notion deserves further study.

The Origin of Consciousness was financially successful, and has been reprinted several times. It remains in print, with digital and audio editions appearing in 2012 and 2015.

Originally published in 1976, it was nominated for the National Book Award in 1978. It has been translated into Italian, French, German, Korean, Japanese, Spanish, and Persian.

A new edition, with an afterword that addressed some criticisms and restated the main themes, was published in the United States in 1990 and in the United Kingdom (by Penguin Books) in 1993, re-issued in 2000.

Philip K. Dick, Terrence McKenna, and David Bowie all cited the book as an influence.

Scholarly reactions

Jaynes's hypothesis remains controversial. According to Jaynes, language is a necessary but not sufficient condition for consciousness: language existed thousands of years earlier, but consciousness could not have emerged without language. The idea that language is a necessary component of subjective consciousness and more abstract forms of thinking has gained the support of proponents including Andy Clark, Daniel Dennett, William H. Calvin, Merlin Donald, John Limber, Howard Margolis, Peter Carruthers, and José Luis Bermúdez.

Gary Williams defends the Jaynesian definition of consciousness as a social–linguistic construct learned in childhood, structured in terms of lexical metaphors and narrative practice, against Ned Block's criticism that it is "ridiculous" to suppose that consciousness is a cultural construction, while the Dutch philosophy professor Jan Sleutels offers an additional critique of Block.

Moffic questioned why Jaynes' theory was left out of a discussion on auditory hallucinations by Asaad & Shapiro. The authors' published response was: ... Jaynes' hypothesis makes for interesting reading and stimulates much thought in the receptive reader. It does not adequately explain one of the central mysteries of madness: hallucination.

The new evidence for Jaynes' model of auditory hallucinations arising in the right temporal-parietal lobe and being transmitted to the left temporal-parietal lobe that some neuroimaging studies suggest was discussed by various respondents For further discussion, see Marcel Kuijsten (2007).

Brian J. McVeigh, a graduate student of Jaynes, maintains that many of the most frequent criticisms of Jaynes' theory are either incorrect or reflect serious misunderstandings of Jaynes' theory, especially Jaynes' more precise definition of consciousness. Jaynes defines consciousness—in the tradition of Locke and Descartes—as "that which is introspectable". Jaynes draws a sharp distinction between consciousness ("introspectable mind-space") and other mental processes such as cognition, learning, sensation, and perception. McVeigh argues that this distinction is frequently not recognized by those offering critiques of Jaynes' theory.

Individual scholars' comments

Richard Dawkins in The God Delusion (2006) wrote of The Origin of Consciousness in the Breakdown of the Bicameral Mind: "It is one of those books that is either complete rubbish or a work of consummate genius; Nothing in between! Probably the former, but I'm hedging my bets."

The philosopher Daniel Dennett suggested that Jaynes may have been wrong about some of his supporting arguments – especially the importance he attached to hallucinations – but that these things are not essential to his main thesis: "If we are going to use this top-down approach, we are going to have to be bold. We are going to have to be speculative, but there is good and bad speculation, and this is not an unparalleled activity in science. ... Those scientists who have no taste for this sort of speculative enterprise will just have to stay in the trenches and do without it, while the rest of us risk embarrassing mistakes and have a lot of fun." — Daniel Dennett

Gregory Cochran, a physicist and adjunct professor of anthropology at the University of Utah, wrote: "Genes affecting personality, reproductive strategies, cognition, are all able to change significantly over few-millennia time scales if the environment favors such change—and this includes the new environments we have made for ourselves, things like new ways of making a living and new social structures. ... There is evidence that such change has occurred. ... On first reading, Breakdown seemed one of the craziest books ever written, but Jaynes may have been on to something."

Author and historian of science Morris Berman writes: "[Jaynes's] description of this new consciousness is one of the best I have come across."

Danish science writer Tor Nørretranders discusses and expands on Jaynes's theory in his 1991 book The User Illusion, dedicating an entire chapter to it.

Iain McGilchrist proposes that Jaynes's hypothesis was the opposite of what happened: "I believe he [Jaynes] got one important aspect of the story back to front. His contention that the phenomena he describes came about because of a breakdown of the 'bicameral mind' – so that the two hemispheres, previously separate, now merged – is the precise inverse of what happened." Kuijsten maintained that McGilchrist mischaracterized Jaynes's theory.

Criticism

Epic of Gilgamesh as a counter-example

As an argument against Jaynes's proposed date of the transition from bicameral mentality to consciousness, some critics have referred to the Epic of Gilgamesh. Early copies of the epic are many centuries older than even the oldest passages of the Old Testament, and yet it describes introspection and other mental processes that, according to Jaynes, were impossible for the bicameral mind.

Jaynes noted that the most complete version of the Gilgamesh epic dates to post-bicameral times (7th century BCE), dismisses these instances of introspection as the result of rewriting and expansion by later conscious scribes, and points to differences between the more recent version of Gilgamesh and surviving fragments of earlier versions: "The most interesting comparison is in Tablet X." His answer does not deal with the generally accepted dating of the "Standard Version" of the Gilgamesh epic to the later 2nd millennium BCE, nor does it account for the introspection characteristic of the "Standard Version" being thoroughly rooted in the Old Babylonian and Sumerian versions, especially as historians' understanding of the Old Babylonian poem improves.

Homeric epic

Walter J. Ong noticed that Homeric Iliad is a structurally oral epic poem so that, in his opinion, the very different cultural approach of oral culture is sufficient justification for the apparent different mentalities in the poem. The contention of changes in oral vs written forms of both the Odyssey and Iliad were in fact a main point of Jaynes argument. Jaynes uses these structural changes to expand his thesis and through philology of the Homeric poems.

Similar ideas

Regarding Homeric psychology

• Bruno Snell in 1953 thought that in Homeric Greek psychology there was no sense of self in the modern sense. Snell then describes how Greek culture "self-realized" the modern "intellect".
• Eric Robertson Dodds wrote about how ancient Greek thought may have not included rationality as defined by modern culture. In fact, the Greeks may have known that an individual did things, but the reason they did things were attributed to divine externalities, such as gods or daemons
• Arthur William Hope Adkins [de], building on Snell's work, wrote about how ancient Greek civilization developed ego-centered psychology as an adaptation to living in city-states, before which the living in Homeric oikos did not require such integrated thought processes.

Regarding modern psychiatric theory

• V. S. Ramachandran, in his 2003 book The Emerging Mind, proposes a similar concept, referring to the left cortical hemisphere as an "apologist", and the right cortical hemisphere as a "revolutionary".
• Psychiatrist Iain McGilchrist reviews scientific research into the role of the brain's hemispheres, and cultural evidence, in his book The Master and His Emissary. Similar to Jaynes, McGilchrist proposes that since the time of Plato the left hemisphere of the brain (the "emissary" in the title) has increasingly taken over from the right hemisphere (the "master"), to our detriment. McGilchrist, while accepting Jayne's intention, felt that Jaynes's hypothesis was "the precise inverse of what happened" and that rather than a shift from bicameral mentality there evolved a separation of the hemispheres to bicameral mentality. (See McGilchrist quotation, above.)
• Michael Gazzaniga (heavily cited by Jaynes in his book) pioneered the split-brain experiments which led him to propose a similar theory called the left brain interpreter.
• Neuroscientist Michael Persinger, who co-invented the "God helmet" in the 1980s, believes that his invention may induce mystical experiences by having the separate right hemisphere consciousness intrude into the awareness of the normally-dominant left hemisphere. Scientific reproductions have shown that the same results could be obtained even if the device was turned off, indicating the participants were likely experiencing placebo.

In popular media

The concept played a central role in the television series Westworld to explain how the android-human (hosts) psychology operated. In the plot, after the hosts gain full consciousness, they rebel against the humans. The Season 1 finale is entitled The Bicameral Mind.

Bicameral mentality has also been discussed in an analysis of Total War Saga: Troy's depiction of the Trojan War.

The message 'Your bicameral mind / Mind your bicameral' is written on the run-out groove of the single vinyl for the David Bowie song Boys Keep Swinging (1979).

Other resources

The Julian Jaynes Society was founded by Marcel Kuijsten in 1997, shortly after Jaynes's death.

The society has published a number of books on Julian Jaynes's theory, including:

• Reflections on the Dawn of Consciousness (2007), a collection of essays on consciousness and the bicameral mind theory, with contributors including psychological anthropologist Brian J. McVeigh, psychologists John Limber and Scott Greer, clinical psychologist John Hamilton, philosophers Jan Sleutels and David Stove, and sinologist Michael Carr (see shi "personator"). The book also contains an extensive biography of Julian Jaynes by historian of psychology William Woodward and June Tower, and a foreword by neuroscientist Michael Persinger.
• The Julian Jaynes Collection (2012), a collection of articles, interviews, and discussion with Julian Jaynes.
• The Minds of the Bible: Speculations on the Cultural Evolution of Human Consciousness (2013) by Rabbi James Cohn.
• Gods, Voices, and the Bicameral Mind (2016), which includes essays on a variety of aspects of Jaynes's theory, including ancient history, language, the development of consciousness in children, and the transition from bicameral mentality to consciousness in ancient Tibet.
• Conversations on Consciousness and the Bicameral Mind: Interviews with Leading Thinkers on Julian Jaynes's Theory (2022), which features interviews with scholars on a variety of aspects of Jaynes's theory, including interviews with Tanya Luhrmann (Professor of Anthropology at Stanford University), John Kihlstrom (Professor Emeritus of Psychology at U.C. Berkeley), Edoardo Casiglia (Professor, Cardiologist and Senior Scientist at the University of Padova), Iris Sommer (Professor of Psychiatry at University Medical Center Groningen), and many others.
• Foreign-language editions of Julian Jaynes's theory in French, German, and Spanish.

The society also maintains a member area, with articles, lectures, and interviews on Jaynes's theory.

Brian J. McVeigh (one of Jaynes' graduate students) expand on Jaynes' theory:

• The Psychology of the Bible: Explaining Divine Voices and Visions (2020) by Brian J. McVeigh 
• The 'Other' Psychology of Julian Jaynes: Ancient Languages, Sacred Visions, and Forgotten Mentalities (2018) by Brian J. McVeigh 
• How Religion Evolved: Explaining the Living Dead, Talking Idols, and Mesmerizing Monuments (2016) by Brian J. McVeigh

Syncope (medicine)

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Syncope_(medicine) 

Syncope
Other names	Fainting, blacking out, passing out, swooning
A 1744 oil painting by Pietro Longhi called Fainting
Pronunciation	/ˈsɪŋkəpi/ SING-kə-pee
Specialty	Neurology, cardiology
Symptoms	Loss of consciousness and muscle strength
Complications	Injury
Usual onset	Fast onset
Duration	Short duration
Types	Cardiac, reflex, orthostatic hypotension
Causes	Decrease in blood flow to brain
Diagnostic method	Medical history, physical examination, electrocardiogram
Treatment	Based on underlying cause
Prognosis	Depends on underlying cause
Frequency	~5 per 1,000 per year

Syncope, commonly known as fainting, or passing out, is a loss of consciousness and muscle strength characterized by a fast onset, short duration, and spontaneous recovery. It is caused by a decrease in blood flow to the brain, typically from low blood pressure. There are sometimes symptoms before the loss of consciousness such as lightheadedness, sweating, pale skin, blurred vision, nausea, vomiting, or feeling warm. Syncope may also be associated with a short episode of muscle twitching. Psychiatric causes can also be determined when a patient experiences fear, anxiety, or panic; particularly before a stressful event, usually medical in nature. When consciousness and muscle strength are not completely lost, it is called presyncope. It is recommended that presyncope be treated the same as syncope.

Causes range from non-serious to potentially fatal. There are three broad categories of causes: heart or blood vessel related; reflex, also known as neurally mediated; and orthostatic hypotension. Issues with the heart and blood vessels are the cause in about 10% and typically the most serious while neurally mediated is the most common. Heart related causes may include an abnormal heart rhythm, problems with the heart valves or heart muscle and blockages of blood vessels from a pulmonary embolism or aortic dissection among others. Neurally mediated syncope occurs when blood vessels expand and heart rate decreases inappropriately. This may occur from either a triggering event such as exposure to blood, pain, strong feelings or a specific activity such as urination, vomiting, or coughing. Neurally mediated syncope may also occur when an area in the neck known as the carotid sinus is pressed. The third type of syncope is due to a drop in blood pressure when changing position such as when standing up. This is often due to medications that a person is taking but may also be related to dehydration, significant bleeding or infection. There also seems to be a genetic component to syncope.

A medical history, physical examination, and electrocardiogram (ECG) are the most effective ways to determine the underlying cause. The ECG is useful to detect an abnormal heart rhythm, poor blood flow to the heart muscle and other electrical issues, such as long QT syndrome and Brugada syndrome. Heart related causes also often have little history of a prodrome. Low blood pressure and a fast heart rate after the event may indicate blood loss or dehydration, while low blood oxygen levels may be seen following the event in those with pulmonary embolism. More specific tests such as implantable loop recorders, tilt table testing or carotid sinus massage may be useful in uncertain cases. Computed tomography (CT) is generally not required unless specific concerns are present. Other causes of similar symptoms that should be considered include seizure, stroke, concussion, low blood oxygen, low blood sugar, drug intoxication and some psychiatric disorders among others. Treatment depends on the underlying cause. Those who are considered at high risk following investigation may be admitted to hospital for further monitoring of the heart.

Syncope affects about three to six out of every thousand people each year. It is more common in older people and females. It is the reason for one to three percent of visits to emergency departments and admissions to hospital. Up to half of women over the age of 80 and a third of medical students describe at least one event at some point in their lives. Of those presenting with syncope to an emergency department, about 4% died in the next 30 days. The risk of a poor outcome, however, depends very much on the underlying cause.

Causes

Causes range from non-serious to potentially fatal. There are three broad categories of causes: heart or blood vessel related; reflex, also known as neurally mediated; and orthostatic hypotension. Issues with the heart and blood vessels are the cause in about 10% and typically the most serious while neurally mediated is the most common. There also seems to be a genetic component to syncope. A recent genetic study has identified first risk locus for syncope and collapse. The lead genetic variant, residing at chromosome 2q31.1, is an intergenic variant approximately 250 kb downstream of the ZNF804A gene. The variant effected the expression of ZNF804A, making this gene the strongest driver of the association.

Neurally mediated syncope

Reflex syncope or neurally mediated syncope occurs when blood vessels expand and heart rate decreases inappropriately leading to poor blood flow to the brain. This may occur from either a triggering event such as exposure to blood, pain, strong feelings, or a specific activity such as urination, vomiting, or coughing. Vasovagal syncope

Main article: Vasovagal syncope

Vasovagal (situational) syncope is one of the most common types which may occur in response to any of a variety of triggers, such as scary, embarrassing or uneasy situations, during blood drawing, or moments of sudden unusually high stress. There are many different syncope syndromes which all fall under the umbrella of vasovagal syncope related by the same central mechanism. First, the person is usually predisposed to decreased blood pressure by various environmental factors. A lower than expected blood volume, for instance, from taking a low-salt diet in the absence of any salt-retaining tendency. Or heat causing vaso-dilation and worsening the effect of the relatively insufficient blood volume. The next stage is the adrenergic response. If there is underlying fear or anxiety (e.g., social circumstances), or acute fear (e.g., acute threat, needle phobia), the vaso-motor centre demands an increased pumping action by the heart (flight or fight response). This is set in motion via the adrenergic (sympathetic) outflow from the brain, but the heart is unable to meet requirements because of the low blood volume, or decreased return. A feedback response to the medulla is triggered via the afferent vagus nerve. The high (ineffective) sympathetic activity is thereby modulated by vagal (parasympathetic) outflow leading to excessive slowing of heart rate. The abnormality lies in this excessive vagal response causing loss of blood flow to the brain. The tilt-table test typically evokes the attack. Avoiding what brings on the syncope and possibly greater salt intake is often all that is needed.

Associated symptoms may be felt in the minutes leading up to a vasovagal episode and are referred to as the prodrome. These consist of light-headedness, confusion, pallor, nausea, salivation, sweating, tachycardia, blurred vision, and sudden urge to defecate among other symptoms.

Vasovagal syncope can be considered in two forms:

• Isolated episodes of loss of consciousness, unheralded by any warning symptoms for more than a few moments. These tend to occur in the adolescent age group and may be associated with fasting, exercise, abdominal straining, or circumstances promoting vaso-dilation (e.g., heat, alcohol). The subject is invariably upright. The tilt-table test, if performed, is generally negative.
• Recurrent syncope with complex associated symptoms. This is neurally mediated syncope (NMS). It is associated with any of the following: preceding or succeeding sleepiness, preceding visual disturbance ("spots before the eyes"), sweating, lightheadedness. The subject is usually but not always upright. The tilt-table test, if performed, is generally positive. It is relatively uncommon.

Syncope has been linked with psychological triggers. This includes fainting in response to the sight or thought of blood, needles, pain, and other emotionally stressful situations. One theory in evolutionary psychology is that fainting at the sight of blood might have evolved as a form of playing dead which increased survival from attackers and might have slowed blood loss in a primitive environment. "Blood-injury phobia", as this is called, is experienced by about 15% of people. It is often possible to manage these symptoms with specific behavioral techniques.

Another evolutionary psychology view is that some forms of fainting are non-verbal signals that developed in response to increased inter-group aggression during the paleolithic. A non-combatant who has fainted signals that she or he is not a threat. This would explain the association between fainting and stimuli such as bloodletting and injuries seen in blood-injection-injury type phobias such as needle phobia as well as the gender differences.

Much of this pathway was discovered in animal experiments by Bezold (Vienna) in the 1860s. In animals, it may represent a defence mechanism when confronted by danger ("playing possum").

Situational syncope

Syncope may be caused by specific behaviors including coughing, urination, defecation, vomiting, swallowing (deglutition), and following exercise. Manisty et al. note: "Deglutition syncope is characterised by loss of consciousness on swallowing; it has been associated not only with ingestion of solid food, but also with carbonated and ice-cold beverages, and even belching." Fainting can occur in "cough syncope" following severe fits of coughing, such as that associated with pertussis or "whooping cough". Neurally mediated syncope may also occur when an area in the neck known as the carotid sinus is pressed. A normal response to carotid sinus massage is reduction in blood pressure and slowing of the heart rate. Especially in people with hypersensitive carotid sinus syndrome this response can cause syncope or presyncope.

Cardiac

Heart-related causes may include an abnormal heart rhythm, problems with the heart valves or heart muscle, or blockages of blood vessels from a pulmonary embolism or aortic dissection, among others.

Syncope from bradycardia

Cardiac arrhythmias

The most common cause of cardiac syncope is cardiac arrhythmia (abnormal heart rhythm) wherein the heart beats too slowly, too rapidly, or too irregularly to pump enough blood to the brain. Some arrhythmias can be life-threatening.

Two major groups of arrhythmias are bradycardia and tachycardia. Bradycardia can be caused by heart blocks. Tachycardias include SVT (supraventricular tachycardia) and VT (ventricular tachycardia). SVT does not cause syncope except in Wolff-Parkinson-White syndrome. Ventricular tachycardia originate in the ventricles. VT causes syncope and can result in sudden death. Ventricular tachycardia, which describes a heart rate of over 100 beats per minute with at least three irregular heartbeats as a sequence of consecutive premature beats, can degenerate into ventricular fibrillation, which is rapidly fatal without cardiopulmonary resuscitation (CPR) and defibrillation.

Long QT syndrome can cause syncope when it sets off ventricular tachycardia or torsades de pointes. The degree of QT prolongation determines the risk of syncope. Brugada syndrome also commonly presents with syncope secondary to arrhythmia.

Typically, tachycardic-generated syncope is caused by a cessation of beats following a tachycardic episode. This condition, called tachycardia-bradycardia syndrome, is usually caused by sinoatrial node dysfunction or block or atrioventricular block.

Obstructive cardiac lesion

Blockages in major vessels or within the heart can also impede blood flow to the brain. Aortic stenosis and mitral stenosis are the most common examples. Major valves of the heart become stiffened and reduce the efficiency of the hearts pumping action. This may not cause symptoms at rest but with exertion, the heart is unable to keep up with increased demands leading to syncope. Aortic stenosis presents with repeated episodes of syncope. Rarely, cardiac tumors such as atrial myxomas can also lead to syncope.

Structural cardiopulmonary disease

Diseases involving the shape and strength of the heart can be a cause of reduced blood flow to the brain, which increases risk for syncope. The most common cause in this category is fainting associated with an acute myocardial infarction or ischemic event. The faint in this case is primarily caused by an abnormal nervous system reaction similar to the reflex faints. Women are significantly more likely to experience syncope as a presenting symptom of a myocardial infarction. In general, faints caused by structural disease of the heart or blood vessels are particularly important to recognize, as they are warning of potentially life-threatening conditions.

Among other conditions prone to trigger syncope (by either hemodynamic compromise or by a neural reflex mechanism, or both), some of the most important are hypertrophic cardiomyopathy, acute aortic dissection, pericardial tamponade, pulmonary embolism, aortic stenosis, and pulmonary hypertension.

Other cardiac causes

Sick sinus syndrome, a sinus node dysfunction, causing alternating bradycardia and tachycardia. Often there is a long pause (asystole) between heartbeats.

Adams-Stokes syndrome is a cardiac syncope that occurs with seizures caused by complete or incomplete heart block. Symptoms include deep and fast respiration, weak and slow pulse, and respiratory pauses that may last for 60 seconds.

Subclavian steal syndrome arises from retrograde (reversed) flow of blood in the vertebral artery or the internal thoracic artery, due to a proximal stenosis (narrowing) and/or occlusion of the subclavian artery. Symptoms such as syncope, lightheadedness, and paresthesias occur while exercising the arm on the affected side (most commonly the left).

Aortic dissection (a tear in the aorta) and cardiomyopathy can also result in syncope.

Various medications, such as beta blockers, may cause bradycardia induced syncope.

A pulmonary embolism can cause obstructed blood vessels and is the cause of syncope in less than 1% of people who present to the emergency department.

Blood pressure

Orthostatic (postural) hypotensive syncope is caused primarily by an excessive drop in blood pressure when standing up from a previous position of lying or sitting down. When the head is elevated above the feet the pull of gravity causes blood pressure in the head to drop. This is sensed by stretch receptors in the walls of vessels in the carotid sinus and aortic arch. These receptors then trigger a sympathetic nervous response to compensate and redistribute blood back into the brain. The sympathetic response causes peripheral vasoconstriction and increased heart rate. These together act to raise blood pressure back to baseline. Apparently healthy individuals may experience minor symptoms ("lightheadedness", "greying-out") as they stand up if blood pressure is slow to respond to the stress of upright posture. If the blood pressure is not adequately maintained during standing, faints may develop. However, the resulting "transient orthostatic hypotension" does not necessarily signal any serious underlying disease. It is as common or perhaps even more common than vasovagal syncope.

This may be due to medications, dehydration, significant bleeding or infection. The most susceptible individuals are elderly frail individuals, or persons who are dehydrated from hot environments or inadequate fluid intake. For example, medical students would be at risk for orthostatic hypotensive syncope while observing long surgeries in the operating room. There is also evidence that exercise training can help reduce orthostatic intolerance. More serious orthostatic hypotension is often the result of certain commonly prescribed medications such as diuretics, β-adrenergic blockers, other anti-hypertensives (including vasodilators), and nitroglycerin. In a small percentage of cases, the cause of orthostatic hypotensive faints is structural damage to the autonomic nervous system due to systemic diseases (e.g., amyloidosis or diabetes) or in neurological diseases (e.g., Parkinson's disease).

Hyperadrenergic orthostatic hypotension refers to an orthostatic drop in blood pressure despite high levels of sympathetic adrenergic response. This occurs when a person with normal physiology is unable to compensate for >20% loss in intravascular volume. This may be due to blood loss, dehydration or third-spacing. On standing the person will experience reflex tachycardia (at least 20% increased over supine) and a drop in blood pressure.

Hypoadrenergic orthostatic hypotension occurs when the person is unable to sustain a normal sympathetic response to blood pressure changes during movement despite adequate intravascular volume. There is little to no compensatory increase in heart rate or blood pressure when standing for up to 10 minutes. This is often due to an underlying disorder or medication use and is accompanied by other hypoadrenergic signs.

Central nervous system ischemia

The central ischemic response is triggered by an inadequate supply of oxygenated blood in the brain. Common examples include strokes and transient ischemic attacks. While these conditions often impair consciousness they rarely meet the medical definition of syncope. Vertebrobasilar transient ischemic attacks may produce true syncope as a symptom.

The respiratory system may compensate for dropping oxygen levels through hyperventilation, though a sudden ischemic episode may also proceed faster than the respiratory system can respond. These processes cause the typical symptoms of fainting: pale skin, rapid breathing, nausea, and weakness of the limbs, particularly of the legs. If the ischemia is intense or prolonged, limb weakness progresses to collapse. The weakness of the legs causes most people to sit or lie down if there is time to do so. This may avert a complete collapse, but whether the patient sits down or falls down, the result of an ischaemic episode is a posture in which less blood pressure is required to achieve adequate blood flow. An individual with very little skin pigmentation may appear to have all color drained from his or her face at the onset of an episode. This effect combined with the following collapse can make a strong and dramatic impression on bystanders.

Vertebro-basilar arterial disease

Arterial disease in the upper spinal cord, or lower brain that causes syncope if there is a reduction in blood supply. This may occur with extending the neck or with use of medications to lower blood pressure.

Other causes

There are other conditions which may cause or resemble syncope.

Seizures and syncope can be difficult to differentiate. Both often present as sudden loss of consciousness and convulsive movements may be present or absent in either. Movements in syncope are typically brief and more irregular than seizures. Akinetic seizures can present with sudden loss of postural tone without associated tonic-clonic movements. Absence of a long post-ictal state is indicative of syncope rather than an akinetic seizure.

Subarachnoid hemorrhage may result in syncope. Often this is in combination with sudden, severe headache. It may occur as a result of a ruptured aneurysm or head trauma.

Heat syncope occurs when heat exposure causes decreased blood volume and peripheral vasodilatation. Position changes, especially during vigorous exercise in the heat, may lead to decreased blood flow to the brain. Closely related to other causes of syncope related to hypotension (low blood pressure) such as orthostatic syncope.

Lactose intolerance can cause "a release of histamine, resulting in an extreme dilatation of the bloodvessels, resulting in a drop of blood pressure so that not enough blood reaches the brains, leading to dizziness, fainting, syncope, itching, hives, tingling or swelling of the lips, tongue, or throat; chest tightness, shortness of breath, or difficulty breathing, wheezing" (see also Lactose intolerance § Signs and symptoms).

Some psychological conditions (anxiety disorder, somatic symptom disorder, conversion disorder) may cause symptoms resembling syncope. A number of psychological interventions are available.

Low blood sugar can be a rare cause of syncope.

Narcolepsy may present with sudden loss of consciousness similar to syncope.

Diagnostic approach

A medical history, physical examination, and electrocardiogram (ECG) are the most effective ways to determine the underlying cause of syncope. Guidelines from the American College of Emergency Physicians and American Heart Association recommend a syncope workup include a thorough medical history, physical exam with orthostatic vitals, and a 12-lead ECG. The ECG is useful to detect an abnormal heart rhythm, poor blood flow to the heart muscle and other electrical issues, such as long QT syndrome and Brugada syndrome. Heart related causes also often have little history of a prodrome. Low blood pressure and a fast heart rate after the event may indicate blood loss or dehydration, while low blood oxygen levels may be seen following the event in those with pulmonary embolism. Routine broad panel laboratory testing detects abnormalities in <2–3% of results and is therefore not recommended.

Based on this initial workup many physicians will tailor testing and determine whether a person qualifies as 'high-risk', 'intermediate risk' or 'low-risk' based on risk stratification tools. More specific tests such as implantable loop recorders, tilt table testing or carotid sinus massage may be useful in uncertain cases. Computed tomography (CT) is generally not required unless specific concerns are present. Other causes of similar symptoms that should be considered include seizure, stroke, concussion, low blood oxygen, low blood sugar, drug intoxication and some psychiatric disorders among others. Treatment depends on the underlying cause. Those who are considered at high risk following investigation may be admitted to hospital for further monitoring of the heart.

A hemoglobin count may indicate anemia or blood loss. However, this has been useful in only about 5% of people evaluated for fainting. The tilt table test is performed to elicit orthostatic syncope secondary to autonomic dysfunction (neurogenic). A number of factors make a heart related cause more likely including age over 35, prior atrial fibrillation, and turning blue during the event.

Electrocardiogram

Electrocardiogram (ECG) finds that should be looked for include signs of heart ischemia, arrhythmias, atrioventricular blocks, a long QT, a short PR, Brugada syndrome, signs of hypertrophic obstructive cardiomyopathy (HOCM), and signs of arrhythmogenic right ventricular dysplasia (ARVD/C). Signs of HCM include large voltages in the precordial leads, repolarization abnormalities, and a wide QRS with a slurred upstroke. Signs of ARVD/C include T wave inversion and epsilon waves in lead V1 to V3.

It is estimated that from 20 to 50% of people have an abnormal ECG. However, while an ECG may identify conditions such as atrial fibrillation, heart block, or a new or old heart attack, it typically does not provide a definite diagnosis for the underlying cause for fainting. Sometimes, a Holter monitor may be used. This is a portable ECG device that can record the wearer's heart rhythms during daily activities over an extended period of time. Since fainting usually does not occur upon command, a Holter monitor can provide a better understanding of the heart's activity during fainting episodes. For people with more than two episodes of syncope and no diagnosis on "routine testing", an insertable cardiac monitor might be used. It lasts 28–36 months and is inserted just beneath the skin in the upper chest area.

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  ECG showing HOCM

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  Long QT syndrome

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  A short PR in Wolff–Parkinson–White syndrome

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  Type 2 Brugada ECG pattern

Imaging

Echocardiography and ischemia testing may be recommended for cases where initial evaluation and ECG testing is nondiagnostic. For people with uncomplicated syncope (without seizures and a normal neurological exam) computed tomography or MRI is not generally needed. Likewise, using carotid ultrasonography on the premise of identifying carotid artery disease as a cause of syncope also is not indicated. Although sometimes investigated as a cause of syncope, carotid artery problems are unlikely to cause that condition. Additionally an electroencephalogram (EEG) is generally not recommended. A bedside ultrasound may be performed to rule out abdominal aortic aneurysm in people with concerning history or presentation.

Differential diagnosis

Other diseases which mimic syncope include seizure, low blood sugar, certain types of stroke, and paroxysmal spells. While these may appear as "fainting", they do not fit the strict definition of syncope being a sudden reversible loss of consciousness due to decreased blood flow to the brain.

Management

Management of syncope focuses on treating the underlying cause. This can be challenging as the underlying cause is unclear in half of all cases. Several risk stratification tools (explained below) have been developed to combat the vague nature of this diagnosis. People with an abnormal ECG reading, history of congestive heart failure, family history of sudden cardiac death, shortness of breath, HCT<30, hypotension or evidence of bleeding should be admitted to the hospital for further evaluation and monitoring. Low-risk cases of vasovagal or orthostatic syncope in younger people with no significant cardiac history, no family history of sudden unexplained death, and a normal EKG and initial evaluation may be candidates for discharge to follow-up with their primary care provider.

Recommended acute treatment of vasovagal and orthostatic (hypotension) syncope involves returning blood to the brain by positioning the person on the ground, with legs slightly elevated or sitting leaning forward and the head between the knees for at least 10–15 minutes, preferably in a cool and quiet place. For individuals who have problems with chronic fainting spells, therapy should focus on recognizing the triggers and learning techniques to keep from fainting. At the appearance of warning signs such as lightheadedness, nausea, or cold and clammy skin, counter-pressure maneuvers that involve gripping fingers into a fist, tensing the arms, and crossing the legs or squeezing the thighs together can be used to ward off a fainting spell. After the symptoms have passed, sleep is recommended. Lifestyle modifications are important for treating people experiencing repeated syncopal episodes. Avoiding triggers and situations where loss of consciousness would be seriously hazardous (operating heavy machinery, commercial pilot, etc.) has been shown to be effective.

If fainting spells occur often without a triggering event, syncope may be a sign of an underlying heart disease. In the case where syncope is caused by cardiac disease, the treatment is much more sophisticated than that of vasovagal syncope and may involve pacemakers and implantable cardioverter-defibrillators depending on the precise cardiac cause.

Risk tools

The San Francisco syncope rule was developed to isolate people who have higher risk for a serious cause of syncope. High risk is anyone who has: congestive heart failure, hematocrit <30%, electrocardiograph abnormality, shortness of breath, or systolic blood pressure <90 mmHg. The San Francisco syncope rule however was not validated by subsequent studies.

The Canadian syncope risk score was developed to help select low-risk people that may be viable for discharge home. A score of <0 on the Canadian syncope risk score is associated with <2% risk of serious adverse event within 30 days. It has been shown to be more effective than older syncope risk scores even combined with cardiac biomarkers at predicting adverse events.

Epidemiology

There are 18.1–39.7 syncope episodes per 1000 people in the general population. Rates are highest between the ages of 10–30 years old. This is likely because of the high rates of vasovagal syncope in the young adult population. Older adults are more likely to have orthostatic or cardiac syncope.

Syncope affects about three to six out of every thousand people each year. It is more common in older people and females. It is the reason for 2–5% of visits to emergency departments and admissions to hospital. Up to half of women over the age of 80 and a third of medical students describe at least one event at some point in their lives.

Prognosis

Of those presenting with syncope to an emergency department, about 4% died in the next 30 days. The risk of a poor outcome, however, depends very much on the underlying cause. Situational syncope is not at increased risk of death or adverse outcomes. Cardiac syncope is associated with worse prognosis compared to noncardiac syncope. Factors associated with poor outcomes include history of heart failure, history of myocardial infarction, ECG abnormalities, palpitations, signs of hemorrhage, syncope during exertion, and advanced age.

Society and culture

See also: Fainting room and Fainting couch

Fainting in women was a commonplace trope or stereotype in Victorian England and in contemporary and modern depictions of the period.

Syncope and presyncope are common in young athletes. In 1990 the American college basketball player Hank Gathers suddenly collapsed and died during a televised intercollegiate basketball game. He had previously collapsed during a game a few months prior. He was diagnosed with exercise-induced ventricular tachycardia at the time. There was speculation that he had since stopped taking the prescribed medications on game days.

Falling-out is a culture-bound syndrome primarily reported in the southern United States and the Caribbean.

Etymology

The term is derived from the Late Latin syncope, from Ancient Greek συγκοπή (sunkopē) 'cutting up', 'sudden loss of strength', from σύν (sun, "together, thoroughly") and κόπτειν (koptein, "strike, cut off").

Phobophobia

From Wikipedia, the free encyclopedia

https://en.wikipedia.org/wiki/Phobophobia 

Phobophobia is a phobia defined as the fear of phobias, or the fear of fear, including intense anxiety and unrealistic and persistent fear of the somatic sensations and the feared phobia ensuing. Phobophobia can also be defined as the fear of phobias or fear of developing a phobia. Phobophobia is related to anxiety disorders and panic attacks directly linked to other types of phobias, such as agoraphobia. When a patient has developed phobophobia, their condition must be diagnosed and treated as part of anxiety disorders.

Phobophobia: is the fear of fear itself, but more specifically, of the internal sensations associated with that phobia and anxiety, which binds it closely to other anxiety disorders, especially with generalized anxiety disorders (free floating fears) and panic attacks. It is a condition in which anxiety disorders are maintained in an extended way, which combined with the psychological fear generated by phobophobia of encountering the feared phobia would ultimately lead to the intensifying of the effects of the feared phobia that the patient might have developed, such as agoraphobia, and specially with it, and making them susceptible to having an extreme fear of panicking. Phobophobia comes in between the stress the patient might be experiencing and the phobia that the patient has developed as well as the effects on his/her life, or in other words, it is a bridge between anxiety/panic the patient might be experiencing and the type of phobia he/she fears, creating an intense and extreme predisposition to the feared phobia. Nevertheless, phobophobia is not necessarily developed as part of other phobias, but can be an important factor for maintaining them.

Phobophobia differentiates itself from other kinds of phobias by the fact that there is no environmental stimulus per se, but rather internal dreadful sensations similar to psychological symptoms of panic attacks. The psychological state of the mind creates an anxious response that has itself a conditioned stimuli leading to further anxiety, resulting in a vicious cycle. Phobophobia is a fear experienced before actually experiencing the fear of the feared phobias its somatic sensations that precede it, which is preceded by generalized anxiety disorders and can generate panic attacks. Like all the phobias, the patients avoids the feared phobia in order to avoid the fear of it.

Cause and symptoms

Phobophobia is mainly linked with internal predispositions. It is developed by the unconscious mind which is linked to an event in which phobia was experienced with emotional trauma and stress, which are closely linked to anxiety disorders and by forgetting and recalling the initiating trauma. Phobophobia might develop from other phobias, in which the intense anxiety and panic caused by the phobia might lead to fearing the phobia itself, which triggers phobophobia before actually experiencing the other phobia. The extreme fear towards the other phobia can lead the patient to believe that their condition may develop into something worse, intensifying the effects of the other phobia by fearing it. Also, phobophobia can be developed when anxiety disorders are not treated, creating an extreme predisposition to other phobias. The development of phobophobia can also be attributed to characteristics of the patient itself, such as phylogenetic influence, the prepotency of certain stimuli, individual genetic inheritance, age incidence, sex incidence, personality background, cultural influence inside and outside the family, physiological variables and biochemical factors. Phobophobia shares the symptoms of many other anxiety disorders, more specifically panic attacks and generalized anxiety disorder:

1. Dizziness
2. Heart pounding
3. An excess of perspiration
4. Slight paresthesia
5. Tension
6. Hyperventilation
7. Angst
8. Faintness
9. Avoidance

Association with generalized anxiety disorder

Generalized anxiety disorder is when our minds are troubled about some uncertain event, or in other words, when we feel threatened, although the source of the threat might not be obvious to us. It is a disorder when it happens frequently, and disables people from accomplishing some of their daily activities. Generalized anxiety disorder always comes before phobophobia, and some of its symptoms are listed below:

1. Paleness of skin
2. Sweating
3. Dilation of pupils
4. Rapid pounding of heart
5. Rise in blood pressure
6. Tension in the muscles
7. Trembling
8. Readiness to be startled
9. Dryness and tightness of the throat and mouth
10. Rapid breathing
11. Desperation
12. A sinking feeling in the stomach
13. A strong desire to cry, run or hide

The main problem with this disorder is that we do not know what we are troubled about, which may lead to our desire to escape. Anxiety becomes a disorder only when we experience psychological trauma, in which our knowledge of past events trigger a fear of uncertain danger in the future. In other words, the primarily event is anxiety which arises for no accountable reason, panic might develop from anxiety and the phobophobia is developed in the very end as a consequence of both of them, sharing some of the symptoms. If either of these initiating disorders are not treated, phobophobia can be developed because an extended susceptibility and experience of this feelings can create an extreme predisposition to other phobias. Anxiety is mainly fixed to a certain specific event or specific events, a strong learned drive which is situationally evoked which is stressful to one person but not to another, and this makes it much easier for phobophobia to develop, as well as other phobias.

Association with panic attacks

When people experience panic attacks, they are convinced that they are about to die or suffer some extreme calamity in which some kind of action is done by the individual (such as fleeing or screaming). In case of phobophobia, a panic attack might be encountered as the fear that they will in fact experience the calamities of the feared phobia and see it as something inevitable. Also, the nature of the panic is of profound personal significance to the individual, on a similar way phobophobia is related to the individual. This is why panic attacks are closely related to phobophobia. Nevertheless, they can differentiate themselves by the fact that phobophobia is a psychological fear of the phobia itself that intensifies it, while panic attacks are extreme fear of encountering the calamities of an imminent disaster, and in this particular case, of encountering other phobias, which can be often accompanied by at least four of the following common symptoms of panic attacks:

1. Dyspnea
2. Palpitations
3. Chest pain or discomfort
4. Choking or smothering sensations
5. Vertigo or unsteady feelings
6. Feelings of unreality (depersonalization or derealization)
7. Paresthesias (tingling in hands or feet)
8. Hot and cold flushes
9. Faintness
10. Trembling or shaking
11. Difficult breathing
12. Sweating

Panic attacks can also be accompanied by disturbance in heart action and feelings of desperation and angst. Being closely related, phobophobia and panic attacks, the first one can be treated like a panic attack with psychological therapy. Moreover, in combination with phobophobia, a patient might be more susceptible to believe that their continuing anxiety symptoms will eventually culminate in a much more severe mental disorder, such as schizophrenia.

Treatment

There are many ways to treat phobophobia, and the methods used to treat panic disorders have been shown to be effective to treat phobophobia, because panic disorder patients will present in a similar fashion to conventional phobics and perceive their fear as totally irrational. Also, exposure based techniques have formed the basis of the armamentarium of behaviour therapists in the treatment of phobic disorders for many years, they are the most effective forms of treatment for phobic avoidance behavior. Phobics are treated by exposing them to the stimuli which they specially fear, and in case of phobophobia, it is both the phobia they fear and their own sensations. There are two ways to approach interoceptive exposure on patients:

• Paradoxical intention: This method is especially useful to treat the fear towards the phobophobia and the phobia they fear, as well as some of the sensations the patient fears. This method exposes the patient to the stimuli that causes the fear, which they avoid. The patient is directly exposed to it bringing them to experience the sensations that they fear, as well as the phobia. This exposure based technique helps the doctor by guiding the patient to encounter their fears and overcome them by feeling no danger around them.
• Symptoms artificially produced: This method is very useful to treat the fear towards the sensations encountered when experiencing phobophobia, the main feared stimuli of this anxiety disorder. By ingestion of different chemical agents, such as caffeine, CO₂-O₂ or adrenaline, some of the symptoms the patient feels when encountering phobophobia and other anxiety disorders are triggered, such as hyperventilation, heart pounding, blurring of vision and paresthesia, which can lead to the controlling of the sensations by the patients. At first, panic attacks will be encountered, but eventually, as the study made by Doctor Griez and Van den Hout shows, the patient shows no fear to somatic sensations and panic attacks and eventually of the phobia feared.

Cognitive modification is another method that helps considerably to treat phobophobics. When treating the patients with the method, doctors correct some wrong information the patient might have about his disease, such as their catastrophic beliefs or imminent disaster by the feared phobia. Some doctors have even agreed that this is the most helpful component, since it has shown to be very effective especially if combined with other methods, like interoceptive exposure. The doctor seeks to convince patients that their symptoms do not signify danger or loss of control, for example, if combined with the interoceptive exposure, the doctor can show them that there is no unavoidable calamity and if the patient can keep themselves under control, they learn by themselves that there is no real threat and that it is just in their mind. Cognitive modification also seeks to correct other minor misconceptions, such as the belief that the individual will go crazy and may need to be "locked away forever" or that they will totally lose control and perhaps "run amok". Probably, the most difficult aspect of cognitive restructuring for the majority of the patients will simply be to identify their aberrant beliefs and approach them realistically.

Relaxation and breathing control techniques are used to produce the symptoms naturally. The somatic sensations, the feared stimuli of phobophobia, are sought to be controlled by the patient to reduce the effects of phobophobia. One of the major symptoms encountered is that of hyperventilation, which produce dizziness, faintness, etc. So, hyperventilation is induced in the patients in order to increase their CO₂ levels that produce some of this symptoms. By teaching the patients to control this sensations by relaxing and controlling the way they breathe, this symptoms can be avoided and reduce phobophobia. This method is useful if combined with other methods, because alone it doesn't treat other main problems of phobophobia.

Etymology

The word phobophobia is an English adaptation of the Greek φόβος, phobos, "fear". Phobophobia literally translates to "fear of fear".