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References (10), cited by (6), recommended articles (6).

Behaviour Research and Therapy

Essay-writing phobia in undergraduates.

In view of the understandably cynical reaction which the above title is likely to evoke in most university teachers, it should immediately be pointed out that it is meant not as a euphemism for student laziness, but quite literally, to denote a fear of preparing written work, which is highly disabling, and can therefore endanger the academic career of able and intelligent undergraduates whose performance is otherwise satisfactory and well-regarded by staff.

The problem should be differentiated from two others, possibly related, but nevertheless distinct. The first is ‘scriptophobia’ (Biran, Augusto and Wilson, 1981) or ‘writing phobia’ (Johnson, Shenoy and Gilmore, 1982), which is an irrational fear of writing in front of another person. Although an underlying fear of shame before someone else may be common to essay-writing phobia and scriptophobia, the presenting problem is different. In the former it is concerned with result of academic work expressed in writing (in the two cases seen, it is perfectly conceivable that the fear would have been just as disabling if the essays had been typed or produced on a word processor); in the latter, with the physical act of writing.

The second is ‘writer's block’ [cf., for example, Nurnberger and Zimmerman (1970), Harris (1974). Passman (1976) and Boice (1982, 1983a, b)]. The distinction here is that whereas essay-writing phobia appears to be clearly phobic in character, and occurs in unpracticed writers, with whom the clinical problem is to start them writing; fear, on the other hand, is not reported to be an essential, or even a usual, feature of writer's block, which occurs in professionals with sometimes extensive writing experience, with whom the clinical problem is to maintain a writing schedule.

A procedure for eliminating writer's block in a college student

J. behav. ther. exp. psychiat., applied analysis of human behavior: an alternative to conventional motivational inferences and unconscious determination in therapeutic programming, behav. ther., contingency contracting as a therapeutic tool in the deceleration of amphetamine use, contingency management in writing and the appearance of creative ideas: implications for the treatment of writing blocks, behav. res. ther., increasing the writing productivity of ‘blocked’ academicians, undergraduate students’ preferences for constructed versus multiple-choice assessment of learning, the significance of the academic word list among esl tertiary students in a malaysian public university, the dreaded essay exam, when a high distinction isn't good enough: a review of perfectionism and self-handicapping, a cognitive behavioural coaching intervention for the treatment of perfectionism and self-handicapping in a nonclinical population, perfectionism and evaluative threat, investigating age-related differences in responses to screening items for internalising disorders in three national surveys.

Epidemiological studies typically report lower prevalence of mental disorders among older adults relative to middle-aged and young adults. A possible explanation is that age-related bias in the screening items of diagnostic instruments leads to older adults being differentially screened out of the full assessment. This study investigated potential age-related bias in screening items for internalising disorders in three epidemiological surveys.

Measurement invariance was estimated for the internalising disorder screening items in the 2007 and 1997 Australian National Survey of Mental Health and Wellbeing, and the 2001–2002 National Epidemiologic Survey on Alcohol and Related Conditions. These surveys assessed mental disorders using the Composite International Diagnostic Interview (CIDI) and the Alcohol Use Disorder and Associated Disabilities Interview Schedule–DSM-IV Version (AUDADIS-IV). A series of multi-group confirmatory factor analyses (CFA) were performed for each survey across older (65–85 years), middle (35–64 years) and young (16–34 years) adults.

Differences between successive CFA models for each survey were negligible, indicating measurement invariance across age groups for the CIDI and AUDADIS-IV screening items.

The number of items and symptoms representing internalising pathology differed between surveys. The samples excluded people in aged-care institutions.

While findings do not rule out that other measurement errors may be present (e.g., age-related bias in the remaining items), these results support the validity of the screening items in the CIDI and AUDADIS-IV. Low prevalence estimates of internalising disorders in older adults are unlikely attributable to differences in response patterns to screening items.

Immediate and delayed effects of subchronic Paraquat exposure during an early differentiation stage in 3D-rat brain cell cultures

Xenobiotic exposure is a risk factor in the etiology of neurodegenerative disease. It was recently hypothesized that restricted exposure during brain development could predispose for a neurodegenerative disease later in life. As neuroinflammation contributes to progressive neurodegeneration, it is suspected that neurodevelopmental xenobiotic exposure could elicit a neuroinflammatory process, which over time may assume a detrimental character.

We investigated the neurotoxic effects of paraquat (PQ) in three-dimensional whole rat brain cell cultures, exposed during an early differentiation stage, comparing immediate effects—directly post exposure—with long-term effects, 20 days after interrupted PQ-administration. Adverse effects and neuroinflammatory responses were assessed by measuring changes in gene- and protein-expression as well as by determining cell morphology changes.

Differentiating neural cultures were highly susceptible to PQ and showed neuronal damage and strong astrogliosis. After the 20-day washout period, neurons partially recovered, whereas astrogliosis persisted, and was accompanied by microglial activation of a neurodegenerative phenotype.

Our data shows that immediate and long-term effects of subchronic PQ-exposure differ. Also, PQ-exposure during this window of extensive neuronal differentiation led to a delayed microglial activation, of a character that could promote further pro-inflammatory signals that enable prolonged inflammation, thereby fueling further neurodegeneration.

Dynamics of Hippocampal Protein Expression During Long-term Spatial Memory Formation

Spatial memory depends on the hippocampus, which is particularly vulnerable to aging. This vulnerability has implications for the impairment of navigation capacities in older people, who may show a marked drop in performance of spatial tasks with advancing age. Contemporary understanding of long-term memory formation relies on molecular mechanisms underlying long-term synaptic plasticity. With memory acquisition, activity-dependent changes occurring in synapses initiate multiple signal transduction pathways enhancing protein turnover. This enhancement facilitates de novo synthesis of plasticity related proteins, crucial factors for establishing persistent long-term synaptic plasticity and forming memory engrams. Extensive studies have been performed to elucidate molecular mechanisms of memory traces formation; however, the identity of plasticity related proteins is still evasive. In this study, we investigated protein turnover in mouse hippocampus during long-term spatial memory formation using the reference memory version of radial arm maze (RAM) paradigm. We identified 1592 proteins, which exhibited a complex picture of expression changes during spatial memory formation. Variable linear decomposition reduced significantly data dimensionality and enriched three principal factors responsible for variance of memory-related protein levels at (1) the initial phase of memory acquisition (165 proteins), (2) during the steep learning improvement (148 proteins), and (3) the final phase of the learning curve (123 proteins). Gene ontology and signaling pathways analysis revealed a clear correlation between memory improvement and learning phase-curbed expression profiles of proteins belonging to specific functional categories. We found differential enrichment of (1) neurotrophic factors signaling pathways, proteins regulating synaptic transmission, and actin microfilament during the first day of the learning curve; (2) transcription and translation machinery, protein trafficking, enhancement of metabolic activity, and Wnt signaling pathway during the steep phase of memory formation; and (3) cytoskeleton organization proteins. Taken together, this study clearly demonstrates dynamic assembly and disassembly of protein-protein interaction networks depending on the stage of memory formation engrams.

Importance of First and Second Authorship in Assessing Citation-Based Scholarly Activity of US Radiation Oncology Residents and Subsequent Choice of Academic Versus Private Practice Career

The Hirsch index (h-index) has been shown to correlate with radiation oncology residents’ having a first job in academics versus private practice, but it is limited by its inability to distinguish between the differing significance of coauthor roles in articles.

A list of 2016 radiation oncology resident graduates and their postresidency career choices was compiled. The Scopus bibliometric citation database was then searched to collect h-index data for articles limited to first author only (h f ) and first or second-author only (h s ) for each resident.

Mean h f was 2.06 for all resident graduates, and mean h s was 2.77. Residents with PhDs had significantly higher h f (3.11 versus 1.76, P < .01) and h s (4.50 versus 2.28, P < .01). There was no statistically significant difference between male and female residents for h f (2.19 versus 1.61, P = .11) or h s (2.91 versus 2.25, P = .15). Residents choosing academia had higher h f (2.72 versus 1.44, P < .01) and h s (3.57 versus 2.01, P < 0.01) than those in private practice. Fewer than 20% of graduates with h f = 0 and only 10% of graduates with h s = 0 secured academic jobs.

The average radiation oncology resident graduate has published a minimum of two first- and/or second-author articles cited at least twice. Graduates with PhDs and/or choosing academic careers were more likely to have higher h f and h s scores; there was no significant score difference by gender. Only 10% of graduates without any first- and/or second-author articles cited at least once secured academic jobs. These findings indicate that stratifying publications by first or second authorship when developing benchmarks for evaluating resident productivity and postresidency career type may be useful.

Development of non-catecholaminergic sympathetic neurons in para- and prevertebral ganglia of cats

Expression of vasoactive intestinal peptide (VIP), neuronal nitric oxide synthase (nNOS), choline acetyltransferase (ChAT) and calcitonin gene-related peptide (CGRP) in the sympathetic ganglia was investigated by immunohistochemistry in the superior cervical ganglion (SCG), stellate ganglion (SG) and celiac ganglion (CG) from cats of different ages (newborn, 10-day-old, 20-day-old, 30-day-old and 2-month-old). Non-catecholaminergic TH-negative VIP-immunoreactive (IR) and nNOS-IR sympathetic ganglionic neurons are present from the moment of birth. In all studied age groups, substantial populations of VIP-IR (up to 9.8%) and nNOS-IR cells (up to 8.3%) was found in the SG, with a much smaller population found in the SCG (<1%) and only few cells observed in the CG. The percentage of nNOS-IR and VIP-IR neurons in the CG and SCG did not significantly change during development. The proportion of nNOS-IR and VIP-IR neuron profiles in the SG increased in first 20 days of life from 2.3 ± 0.15% to 8.3 ± 0.56% and from 0.3 ± 0.05% to 9.2 ± 0.83%, respectively. In the SG, percentages of nNOS-IR sympathetic neurons colocalizing VIP increased in the first 20 days of life. ChAT-IR and CGRP-IR neurons were not observed in the sympathetic ganglia of newborn animals and did not appear until 10 days after birth. In the SG of newborn and 10-day-old kittens, the majority of NOS-IR neurons were calbindin (CB)-IR, whereas in the SCG and CG of cats of all age groups and in the SG of 30-day-old and older kittens, the vast majority of NOS-IR neurons lacked CB. We conclude that the development of various non-catecholaminergic neurons in different sympathetic ganglia has its own time dynamics and is concluded at the end of the second month of life.

A PCR-RFLP method for the simultaneous differentiation of three Entamoeba species

Amoebiasis caused by Entamoeba histolytica continues to be one of the most common parasitic diseases in the developing world. Despite its relevance, due to the lack of accurate diagnostic methods, the true clinical and public health importance of this parasite remains uncertain. The aim of this study was to develop a new diagnostic tool to differentiate E. histolytica from the morphologically undistinguishable E. dispar and E. moshkovskii . We developed a specific, fast and simple PCR-RFLP method that was able to accurately differentiate experimentally-obtained restriction patterns from the three Entamoeba species. This new method could prove useful for clinical and epidemiological purposes.

Home — Essay Samples — Psychology — Phobias — An Analysis of the Origin of Phobias

An Analysis of The Origin of Phobias

Why do people have phobias?

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Everything you need to know about phobias

phobia essay pdf

A phobia is a type of anxiety disorder that causes an individual to experience extreme, irrational fear about a situation, living creature, place, or object.

When a person has a phobia, they will often shape their lives to avoid what they consider to be dangerous. The imagined threat is greater than any actual threat posed by the cause of terror.

Phobias are diagnosable mental disorders.

The person will experience intense distress when faced with the source of their phobia. This can prevent them from functioning normally and sometimes leads to panic attacks .

In the United States, approximately 19 million people have phobias.

What is a phobia?

Phobia face woman

A phobia is an exaggerated and irrational fear.

The term ‘phobia’ is often used to refer to a fear of one particular trigger. However, there are three types of phobia recognized by the American Psychiatric Association (APA). These include:

Specific phobia: This is an intense, irrational fear of a specific trigger.

Social phobia, or social anxiety : This is a profound fear of public humiliation and being singled out or judged by others in a social situation. The idea of large social gatherings is terrifying for someone with social anxiety . It is not the same as shyness.

Agoraphobia: This is a fear of situations from which it would be difficult to escape if a person were to experience extreme panic, such being in a lift or being outside of the home. It is commonly misunderstood as a fear of open spaces but could also apply to being confined in a small space, such as an elevator, or being on public transport. People with agoraphobia have an increased risk of panic disorder.

Specific phobias are known as simple phobias as they can be linked to an identifiable cause that may not frequently occur in the everyday life of an individual, such as snakes. These are therefore not likely to affect day-to-day living in a significant way.

Social anxiety and agoraphobia are known as complex phobias, as their triggers are less easily recognized. People with complex phobias can also find it harder to avoid triggers, such as leaving the house or being in a large crowd.

A phobia becomes diagnosable when a person begins organizing their lives around avoiding the cause of their fear. It is more severe than a normal fear reaction. People with a phobia have an overpowering need to avoid anything that triggers their anxiety.

A person with a phobia will experience the following symptoms. They are common across the majority of phobias:

A person is likely to experience feelings of panic and intense anxiety when exposed to the object of their phobia. The physical effects of these sensations can include:

A feeling of anxiety can be produced simply by thinking about the object of the phobia. In younger children, parents may observe that they cry, become very clingy, or attempt to hide behind the legs of a parent or an object. They may also throw tantrums to show their distress.

Complex phobias

A complex phobia is much more likely to affect a person’s wellbeing than a specific phobia.

For example, those who experience agoraphobia may also have a number of other phobias that are connected. These can include monophobia, or a fear of being left alone, and claustrophobia , a fear of feeling trapped in closed spaces.

In severe cases, a person with agoraphobia will rarely leave their home.

The most common specific phobias in the U.S. include:

These are far from the only specific phobias. People can develop a phobia of almost anything. Also, as society changes, the list of potential phobias changes. For instance, nomophobia is the fear of being without a cell phone or computer.

As described in one paper , it is “the pathologic fear of remaining out of touch with technology.”

It is unusual for a phobia to start after the age of 30 years, and most begin during early childhood, the teenage years, or early adulthood.

They can be caused by a stressful experience, a frightening event, or a parent or household member with a phobia that a child can ‘learn.’

Specific phobias

These usually develop before the age of 4 to 8 years. In some cases, it may be the result of a traumatic early experience. One example would be claustrophobia developing over time after a younger child has an unpleasant experience in a confined space.

Phobias that start during childhood can also be caused by witnessing the phobia of a family member. A child whose mother has arachnophobia, for example, is much more likely to develop the same phobia.

More research is needed to confirm exactly why a person develops agoraphobia or social anxiety. Researchers currently believe complex phobias are caused by a combination of life experiences, brain chemistry, and genetics.

They may also be an echo of the habits of early humans, leftover from a time in which open spaces and unknown people generally posed a far greater threat to personal safety than in today’s world.

How the brain works during a phobia

Some areas of the brain store and recall dangerous or potentially deadly events.

If a person faces a similar event later on in life, those areas of the brain retrieve the stressful memory, sometimes more than once. This causes the body to experience the same reaction.

In a phobia, the areas of the brain that deal with fear and stress keep retrieving the frightening event inappropriately.

Researchers have found that phobias are often linked to the amygdala , which lies behind the pituitary gland in the brain. The amygdala can trigger the release of “fight-or-flight” hormones. These put the body and mind in a highly alert and stressed state.

Phobias are highly treatable, and people who have them are nearly always aware of their disorder. This helps diagnosis a great deal.

Speaking to a psychologist or psychiatrist is a useful first step in treating a phobia that has already been identified.

If the phobia does not cause severe problems, most people find that simply avoiding the source of their fear helps them stay in control. Many people with specific phobias will not seek treatment as these fears are often manageable.

It is not possible to avoid the triggers of some phobias, as is often the case with complex phobias. In these cases, speaking to a mental health professional can be the first step to recovery.

Most phobias can be cured with appropriate treatment. There is no single treatment that works for every person with a phobia. Treatment needs to be tailored to the individual for it to work.

The doctor, psychiatrist, or psychologist may recommend behavioral therapy, medications, or a combination of both. Therapy is aimed at reducing fear and anxiety symptoms and helping people manage their reactions to the object of their phobia.

Medications

The following medications are effective for the treatment of phobias.

These can help reduce the physical signs of anxiety that can accompany a phobia.

Side effects may include an upset stomach , fatigue , insomnia , and cold fingers.

Antidepressants

Serotonin reuptake inhibitors (SSRIs) are commonly prescribed for people with phobias. They affect serotonin levels in the brain, and this can result in better moods.

SSRIs may initially cause nausea, sleeping problems, and headaches.

If the SSRI does not work, the doctor may prescribe a monoamine oxidase inhibitor (MAOI) for social phobia. Individuals on an MAOI may have to avoid certain types of food. Side effects may initially include dizziness, an upset stomach, restlessness, headaches, and insomnia.

Taking a tricyclic antidepressant (TCA), such as clomipramine, or Anafranil, has also been found to help phobia symptoms. Initial side effects can include sleepiness, blurred vision, constipation , urination difficulties, irregular heartbeat, dry mouth, and tremors.

Benzodiazepines are an example of a tranquilizer that might be prescribed for a phobia. These may help reduce anxiety symptoms. People with a history of alcohol dependence should not be given sedatives.

In 2020, the Food and Drug Administration (FDA) strengthened their warning about benzodiazepines. Using these drugs can lead to physical dependence, and withdrawal can be life threatening. Combining them with alcohol, opioids, and other substances can result in death. It is essential to follow the doctor’s instructions when using these drugs.

Behavioral therapy

There are a number of therapeutic options for treating a phobia.

Desensitization, or exposure therapy

This can help people with a phobia alter their response to the source of fear. They are gradually exposed to the cause of their phobia over a series of escalating steps. For example, a person with aerophobia, or a fear of flying on a plane, may take the following steps under guidance:

Cognitive behavioral therapy (CBT)

The doctor, therapist, or counselor helps the person with a phobia learn different ways of understanding and reacting to the source of their phobia. This can make coping easier. Most importantly, CBT can teach a person experiencing phobia to control their own feelings and thoughts.

Phobias can be a source of genuine and ongoing distress for an individual. However, they are treatable in most cases, and very often the source of fear is avoidable.

If you have a phobia, the one thing you should never be afraid of is seeking help. The Anxiety and Depression Association of America (ADAA) offer a useful resource for locating a therapist . They also offer a range of talks on how to overcome specific phobias.

Last medically reviewed on December 19, 2017

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Related Coverage

A phobia is a type of anxiety disorder. It causes a person to experience an overwhelming or debilitating fear of a situation or thing. Learn more here.

Claustrophobia is a type of anxiety disorder, in which an irrational fear of being unable to escape from a small, enclosed environment can lead to a…

Agoraphobia is an anxiety disorder. It can cause intense fear in situations where escape may be difficult or help hard to access. Learn about…

Arachnophobia is an extreme fear of spiders and other arachnids. It is one of the more common types of phobias. Learn more.

Acrophobia is an intense fear of heights. If a person has acrophobia, being high up or thinking about heights may cause them to have a panic attack…

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