Claustrophobia
CLAUSTROPHOBIA
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| Claustrophobic Person |
Disadvantages Of Claustrophobia
A phobia is
an extreme state of fear of something. Currently, many types of phobia have
been identified. The most common of these is claustrophobia. Claustrophobia is
a problem that affects people's lives and
it has many disadvantages.
The biggest
disadvantage is that people can not be found in small spaces. Claustrophobic
people can't stay in narrow spaces. This situation prevents them from go to
some places. They can't even stay in their own rooms if they experience too
much stress during the day. I even think advanced level claustrophobic people
can not even sleep in bunk beds.
Another
disadvantage is high buildings. Nowadays, there are very high buildings and it
is impossible to reach the upper floors without using an elevator. Claustrophobic
people can not live in buildings like this because they can't get on an
elevator. Sometimes they can't get into the building when they go for a job interview or a meeting and that makes their life
difficult.
Thirdly,
claustrophobic people can not be found in crowded
places. Even if they are outdoors, they cannot be in this environment if the
environment is crowded. People with claustrophobia may experience panic attacks
by getting stressed in crowded environments. Therefore, they can not attend
events such as concerts, theatre, cinema and parties.
people who
experience mild claustrophobia can cope with these disadvantages but people
with advanced claustrophobia can not get over it easily. Their lives are both
partially hindered and they live by avoiding
such situations. These disadvantages make their lives very difficult.
Treatments Of
Claustrophobia
Phobia is the
extreme way of fear. It affects people's lives and puts them in a hard
situation to deal with. Nowadays, lots of phobia type have been found. The most
known is claustrophobia. Claustrophobia is a fear of being in a confined area.
There are some treatment methods for
claustrophobia. However, they are not an exact solution to solve this fear.
People try but these treatment methods can work on some people not all of them.
The most common of
these treatments are breathing exercises. Breathing
exercises regulate heart rhythm and help a
person think logically during stress. People who experience panic attacks do
breathing exercises and this works for many people. It is a very important
treatment method.
Another method of
treatment is stress relieving pills. In some claustrophobic people, simple
methods like breathing exercise don't work. So, they apply a different
treatment and use medication. This method greatly heals people.
The third method
of treatment is to meet with a psychologist. In this method of treatment, the
person regularly goes to the psychologist and the psychologist tries to relieve
the person's anxiety and stress. This is not
a treatment that works for everyone but it must be tried before using the pill.
As a result, there
are different methods of treatment for claustrophobia. Such as medication,
psychologist help, breathing exercises. A claustrophobic person should try to
find out which treatment method is appropriate. People who find the suitable treatment
way reduce the effects of claustrophobia. Continuous treatment can beat
claustrophobia.
“The Mind Is Its Own Place”: Amelioration of Claustrophobia in Semantic Dementia
1. Introduction
Specific phobia is defined in DSM-IVR as marked, persistent, and excessive or unreasonable fear when in the presence of, or when anticipating an encounter with, a specific object or situation [1]. Examples of specific phobias include animals (commonly mice, snakes, and spiders), natural environments (including heights, storms, or water), breaches of one's physical integrity (blood, injections and injury) and situations (notably, closed spaces or claustrophobia). Specific phobias are collectively common, with an estimated lifetime prevalence of around 10% in Western populations [1]. As rare instances of powerfully arousing, intensely fearful stimuli that are regularly encountered in modern developed societies, phobias hold potentially unique insights for our understanding of the cognitive and neural machinery of fear.
Functional imaging in human subjects suggests that specific phobias are neuroanatomically mediated by limbic and paralimbic circuitry including the amygdala, anterior cingulate, insula and dorsolateral prefrontal cortex, and subcortical connections to the ventral striatum and brainstem nuclei including locus coeruleus [2–6]. These brain regions are involved in the representation and interpretation of the phobic object, in amplification of the phobic response, and generation of the characteristic somatic correlates of extreme fear. Proximity of the phobic stimulus modulates activation in stria terminalis and orbitofrontal cortex, while mismatch between predicted and experienced fear engages the amygdala [2]. Supraliminally presented stimuli activate amygdala bilaterally whereas subliminally presented stimuli demonstrate lateralised activity in the right amygdala suggesting a role of the latter in hypervigilance to phobic stimuli before these attain conscious awareness [4]. The role of the amygdala is further underlined by the unique Urbach-Wiethe syndrome in which selective amygdalar proteinosis is accompanied by loss of fear responses [7]. Particular phobias vary in the extent to which they engage cognitive and autonomic components of the fear response [8, 9].
The frontotemporal lobar degenerations (FTLD) are a diverse group of proteinopathies that present clinically with impairments of social conduct and understanding, aphasias or deficits of conceptual knowledge about the world at large [10]. These diseases share a propensity to produce selective brain network disintegration maximally affecting the frontal and anterior temporal lobes [10]. Abnormal reactivity to and comprehension of a range of emotional stimuli are a hallmark of FTLD and in particular the canonical syndromic subtypes of behavioural variant frontotemporal dementia and semantic dementia (SemD). These deficits of emotion processing have been linked to regional atrophy and altered connectivity in frontolimbic circuitry, including orbitofrontal cortex, ventral striatum, insula, and amygdala [10–12]. The SemD syndrome is of particular interest because it is underpinned by selective erosion of semantic memory: the human memory system that governs conceptual and encyclopaedic knowledge about words and objects based on an individual's accumulated experience of the world. SemD is associated with progressive degeneration of a specific brain network centred on the anterior temporal lobes and their connections with inferior frontal, limbic, and more posterior brain regions [13]. SemD is most often led by loss of understanding of word meanings (progressive semantic aphasia) but less commonly can be led by deficits of nonverbal semantic memory, such as impaired face recognition (progressive associative prosopagnosia) [14]. Even in patients presenting with verbal semantic deficits, nonverbal semantic deficits are often detectable [15], and both verbal and nonverbal deficits progress as SemD unfolds, underlining the status of this syndrome as the paradigmatic disorder of the semantic memory system. It is increasingly recognised that SemD is associated with a range of behavioural disturbances that may be at least partly underpinned by severe deficits in comprehending affect-laden as well as affectively neutral objects and social concepts [12, 16, 17].
Here we describe the case of a patient in whom development of SemD was accompanied by striking attenuation of previously disabling claustrophobia, with implications both for our understanding of the pathophysiology of SemD and the brain basis of specific phobias.
2. General Clinical Details
This 71-year-old right-handed retired medical secretary, LC, presented with a seven-year history of cognitive decline led by progressive difficulty recognising familiar faces. More recently she had been unable to recognise even close friends and relatives and increasingly relied on other cues to their personal identity (e.g., the type of car they drove). She had also experienced difficulty recognising voices over the telephone. Word finding difficulties were an early feature and she struggled in particular to retrieve personal and brand names. Increasingly she seemed unable to understand how to use everyday household items or to comprehend environmental sounds. Her family had noted an insidious change in her personality and social behaviour beginning around three years after the onset of prosopagnosia and characterised by development of a sweet tooth, reduced empathy, loss of humour and social sensitivity, and increasing self-centredness, with obsessionality around time-keeping, picture puzzles, and music. There was no history of topographical disorientation. There was a past history of severe claustrophobia with previous psychiatric contact but no other significant past personal or family history.
Neuropsychological assessment (summarised in Table 1) corroborated the clinical impression: LC showed deficits of famous face recognition and visual object identification, anomia, and reduced single word comprehension, but her speech was fluent and normally constructed and there was relative preservation of her mnestic, perceptual and executive functions. The general neurological examination was unremarkable. Brain MRI (Figure 1) showed selective atrophy predominantly affecting the anteroinferior and mesial temporal lobes, more marked in the right hemisphere, with less marked atrophy of perisylvian cortices bilaterally. Based on LC's characteristic neuropsychological and neuroanatomical phenotype, a clinical diagnosis of SemD presenting with progressive prosopagnosia was made. This clinical diagnosis was additionally in line with current consensus criteria for the semantic variant of progressive aphasia, acknowledging that a minority of patients in this group do present with prominent difficulties with person recognition [13].
3. Alterations in Claustrophobia and Other Emotional Responses
A noteworthy feature of LC's history was striking attenuation of her previously disabling, longstanding claustrophobia following the onset of cognitive decline. She had been diagnosed by a psychiatrist with claustrophobia in her mid-twenties, and this had remained a significant issue throughout her adult life. Even in childhood, she had disliked being in crowded places such as the school chapel, and in her late teens and early twenties she exhibited mounting anxiety when in confined spaces including lifts, trains, aeroplanes, and other situations with no obvious route of escape. She would develop full-blown panic symptoms with sustained exposure to such situations and avoided them wherever possible, sometimes at the cost of considerable inconvenience (e.g., driving many kilometres out of her way to avoid road tunnels or planning vacations around her fear). There had been no suggestion of a generalised anxiety disorder nor any history of other phobic responses. Her family reported that LC's claustrophobia settled within several years of onset of her cognitive symptoms: she would, for example, now travel willingly on the London Underground and enter crowded lifts when accessing the platforms. A compelling illustration occurred some six years following symptom onset, when she agreed to have a brain MRI and underwent the procedure with no evidence of distress. Indeed, her family remarked that loss of her claustrophobia was the one positive outcome of LC's SemD diagnosis.
On specific enquiry, there was the suggestion of a more general alteration in LC's emotional responses. In earlier life she had been prone to fairly regular vociferous, angry outbursts; these had abated following the onset of cognitive decline. In addition, she now failed to react to situations likely to have provoked disgust premorbidly (e.g., leaving her washing machine filled with stagnant water and accumulating cartons of mouldy food in her house). In contrast to this reduction in certain strong premorbid emotional responses, LC had developed a craving for music (musicophilia), repeatedly requesting to hear the same repertoire of songs derived from Hollywood musicals. She evidently derived considerable pleasure from these songs and, before her family intervened, would stay up late into the night listening to them.
4. Discussion
This patient with SemD lost phobic responses to a specific situation (confined spaces) that had previously reliably evoked them, following the onset of her cognitive syndrome. Although this amelioration of claustrophobia probably occurred in the context of a more generalised alteration of strong emotional responsivity, it is nevertheless a striking illustration of the specific modulation of an established behavioural programme by neurodegenerative disease. This case has implications both for our understanding of brain network disintegration in SemD and the neurocognitive basis of phobias more generally.
From a disease perspective, this case shows that the well-recognised effects of SemD on emotion processing extend even to essentially “automatic” and powerful emotional behaviours (such as phobic responses) that have become highly entrenched over the course of a lifetime. While gratifying in this particular patient, there is clear potential for harm here: whereas phobias per se are a nonuseful legacy of our evolutionary past, the capacity to experience fear when confronted with genuinely threatening scenarios remains highly useful. If SemD is accompanied by a more generalised fearlessness, this could leave patients vulnerable in their daily lives: however, there remain few data on the real life impact of altered emotion processing in patients with neurodegenerative diseases [12, 16, 28, 29]. Pathophysiologically, while direct neuroanatomical correlation was not possible here, the pattern of regional brain atrophy exhibited by LC (see Figure 1) suggests that her loss of phobic responses is attributable to involvement of key structures such as the amygdala, insula, and their connections. Aversive learning paradigms in neurodegenerative dementia cohorts have shown that FTLD (in contrast to Alzheimer's disease) is associated both with blunted fear conditioning and reduced autonomic responsivity, and this is in turn correlated with grey matter loss in a large-scale emotion processing network including anterior cingulate, orbitofrontal cortex, and insula [30]. The development of musicophilia in LC's case suggests that SemD does not simply produce a global attenuation of emotionality: rather the specific stimulus may modulate the valence of the abnormal emotional response, presumably owing to stimulus-dependent alterations of connectivity in cognitive and limbic circuitry, as proposed in previous cases of musicophilia associated with SemD [31].
From a neurocognitive perspective, the present case particularly implicates the right temporal lobe in the modulation of phobic responses (since loss of claustrophobia in this case evolved in tandem with prosopagnosia and predominantly right-sided anterior temporal lobe atrophy) and raises the further possibility that the phenomenology of a phobia reflects conjoint processing of both the experience of strong emotion [32] and the cognitive “meaning” of the experience. Moral sentiments experienced by healthy individuals have been shown to be mediated through emotion-specific functional connectivity between the anterior temporal lobe and frontolimbic regions, providing a potential mechanism for conceptual-emotional integration [33]. Disease-associated neuronal dysfunction and loss in SemD affect both temporal and frontal lobe neocortex as well as the subcortical machinery of autonomic responses. We speculate that neocortical processing in the otherwise healthy brain underpins the more complex aspects of phobic behaviour (such as LC's elaborate premorbid avoidance strategies), while impaired neocortical processing (e.g., following onset of SemD) may remove the cognitive significance of the phobic situation along with its autonomic resonance. It may be that attenuation of both these components of the phobic experience is required to “cure” the phobia, as indeed psychologically based treatment strategies would suggest [34, 35].
Conclusions based on single case studies must necessarily be tentative. However we hope that our observations in this case will motivate a further systematic neuropsychological and psychophysical investigation of phobic (and potentially phobic) responses in patients with FTLD, in relation to other neurodegenerative diseases and with electrophysiological and neuroimaging correlation. More philosophically, our case illustrates how the brain constructs a private model of the world and invests this with emotional significance and how this process can be modulated by pathological mental states, as recognised long ago by Milton [36] and others.
What's to know about claustrophobia?
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Claustrophobia is a form of anxiety disorder, in which an irrational fear of having no escape or being closed-in can lead to a panic attack.
It is considered a specific phobia according to the Diagnostic and Statistical Manual 5 (DSM-5).
Triggers may include being inside an elevator, a small room without any windows, or even being on an airplane.
Some people have reported that wearing tight-necked clothing can provoke feelings of claustrophobia.
Fast facts on claustrophobia:
Here are some key points about claustrophobia. More detail is in the main article.
- Claustrophobia affects some people when they are in a small space.
- It can lead to feelings of panic.
- Causes may include conditioning and genetic factors.
- A variety of tips and treatments may help people overcome their fear.
The word claustrophobia comes from the Latin word claustrum which means “a closed-in place,” and the Greek word, phobos meaning “fear.”
People with claustrophobia will go to great lengths to avoid small spaces and situations that trigger their panic and anxiety.
They may avoid places like the subway and prefer to take the stairs rather than an elevator, even if many floors are involved.
Up to 5 percent of Americans may experience claustrophobia.
Symptoms may be severe, but many people do not seek treatment.
A psychologist or psychiatrist will ask the patient about their symptoms.
A diagnosis of claustrophobia may emerge during a consultation about another anxiety-related issue.
The psychologist will:
- ask for a description of the symptoms and what triggers them
- try to establish how severe the symptoms are
- rule out other types of anxiety disorder
To establish some details, the doctor may use:
- a claustrophobia questionnaire to help identify the cause of anxiety
- a claustrophobia scale to help establish the levels of anxiety
For a specific phobia to be diagnosed, certain criteria need to be met.
These are:
- a persistent unreasonable or excessive fear caused by the presence or anticipation of a specific situation
- anxiety response when exposed to the stimulus, possibly a panic attack in adults, or, in children, a tantrum, clinging, crying or freezing
- a recognition by adult patients that their fear is out of proportion to the perceived threat or danger
- employing measures to avoid the feared object or situation, or a tendency to face the experiences but with distress or anxiety
- the person’s reaction, anticipation or avoidance interferes with everyday life and relationships or causes significant distress
- the phobia has persisted for some time, usually 6 months or longer
- symptoms cannot be attributed to another mental condition, such as obsessive-compulsive disorder (OCD) or post-traumatic stress disorder (PTSD)
Claustrophobia is an anxiety disorder. Symptoms usually appear during childhood or adolescence.
Being in or thinking about being in a confined space can trigger fears of not being able to breathe properly, running out of oxygen, and distress at being restricted.
When anxiety levels reach a certain level, the person may start to experience:
- sweating and chills
- accelerated heart rate and high blood pressure
- dizziness, fainting, and lightheadedness
- dry mouth
- hyperventilation, or “over breathing”
- hot flashes
- shaking or trembling and a sense of “butterflies” in the stomach
- nausea
- headache
- numbness
- a choking sensation
- tightness in the chest, chest pain, and difficulty breathing
- an urge to use the bathroom
- confusion or disorientation
- fear of harm or illness
It is not necessarily the small spaces that trigger the anxiety, but the fear of what can happen to the person if confined to that area.
This is why the person fears running out of oxygen.
Examples of small spaces that could trigger anxiety are:
- elevators or changing rooms in stores
- tunnels, basements, or cellars
- trains and subway trains
- revolving doors
- airplanes
- public toilets
- cars, especially those with central locking
- crowded areas
- automatic car-washes
- some medical facilities, such as MRI scanners
- small rooms, locked rooms, or rooms with windows that do not open
Reactions include:
- checking the exits and staying near them when entering a room
- feeling anxious when all the doors are closed
- staying near the door in a crowded party or gathering
- avoiding driving or traveling as a passenger when traffic is likely to be congested
- using the stairs instead of the elevator, even if this is difficult and uncomfortable
Claustrophobia involves a fear of being restricted or confined to one area, so, having to wait in line at a checkout may also cause it in some people.
Following a diagnosis, the psychologist may recommend one or more of the following treatment options.
Cognitive behavioral therapy (CBT): The aim is to retrain the patient’s mind so that they no longer feel threatened by the places they fear.
It may involve slowly exposing the patient to small spaces and helping them deal with their fear and anxiety.
Having to face the situation that causes the fear may deter people from seeking treatment.
Observing others: Seeing others interact with the source of fear may reassure the patient.
Drug therapy: Antidepressants and relaxants can help manage symptoms, but will not solve the underlying problem.
Relaxation and visualization exercises: Taking deep breaths, meditating and doing muscle-relaxing exercises can help deal with negative thoughts and anxiety.
Alternative or complementary medicine: Some supplements and natural products may help patients manage panic and anxiety. Some calming oils are available for purchase online, such as lavender oil or “rescue remedies”.
Treatment often lasts around 10 weeks, with sessions twice a week. With appropriate treatment, it is possible to overcome claustrophobia.
Tips for coping
Strategies that can help people cope with claustrophobia include:
- staying put if an attack happens. If driving, this may include pulling over to the side of the road and waiting till symptoms have passed.
- reminding yourself that the frightening thoughts and feelings will pass
- trying to focus on something that is not threatening, for example, the time passing or other people
- breathing slowly and deeply, counting to three on each breath
- challenging the fear by reminding yourself that it is not real
- visualizing positive outcomes and images
Longer-term strategies may include joining a yoga class, working out an exercise program, or booking an aromatherapy massage, to help cope with stress.
Past or childhood experience is often the trigger that causes a person to associate small spaces with a sense of panic or imminent danger.
Experiences that can have this effect may include:
- being trapped or kept in a confined place, by accident or on purpose
- being abused or bullied as a child
- getting separated from parents or friends when in a crowded area
- having a parent with claustrophobia
The trauma experienced at that time will affect the person’s ability to cope with a similar situation rationally in future. This is known as classic conditioning.
The person’s mind is believed to link the small space or confined area with the feeling of being in danger. The body then reacts accordingly, or in a way that seems logical.
Classic conditioning can also be inherited from parents or peers. If a parent, for example, has a fear of being close in, the child may observe their behavior and develop the same fears.
Possible genetic or physical factors
Other theories that may explain claustrophobia include:
Having a smaller amygdala: This is the part of the brain that controls how the body
Genetic factors: A dormant evolutionary survival mechanism causes reactions that are no longer needed in today’s world.
Mouse studies
One group of researchers has suggested that people who experience claustrophobia perceive things as being nearer than they are, and that this triggers a defense mechanism.
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