What are anxiety and stressor-related problems? - Chapter 6

What are anxiety disorders?

An anxiety disorder is “an excessive or aroused state characterized by feelings of apprehension, uncertainty and fear” (Davey, 1993). An anxiety response might not be in proportion to a certain threat or may be a state experienced that is not triggered by any obvious threat and may disrupt the ability of an individual to live a normal life due to constant emotional distress. Six of the main anxiety disorders discussed in this chapter are: specific phobias, social anxiety disorder, panic disorder, generalized-anxiety disorder (GAD), obsessive-compulsive disorder (OCD), and post-traumatic stress disorder (PTSD). The diagnosis is based on subjective experience of anxiety that occurs so regularly that it disturbs every-day living.

What is comorbidity?

An individual experiences comorbidity if they experience several anxieties disorders whose symptoms overlap and this occurs quite frequently in anxiety-disorders. Diagnostic categories share common aspects:

• Physiological symptoms are present in panic disorder and in specific phobias
• Cognitive biases play a role in most anxiety disorders
• Dysfunctional perseveration plays a role in various prominent psychopathologies
• In many anxiety disorders certain early experiences are part of the aetiology

What are Specific Phobias and what is their prevalence?

An individual who reacts with unreasonable, excessive and persistent fear to a specific object or situation suffers from specific phobia. Even though the individual is aware of the irrationality of their fear, they have dysfunctional phobic beliefs that explain reasons for why they are afraid and react how they do. In therapy these beliefs can be challenged. Specific phobias are quite common, and recent surveys have suggested that 20% of all adults will experience some sort of diagnosable specific phobia in their life. Women have a lifetime prevalence of 16%, which is higher than the men's 7% lifetime prevalence.

Common phobias include animal phobias (snakes, spider, rats, mice, creepy-crawlies), social anxiety disorder, dental phobia, water phobia, height phobia, claustrophobia, and BII (blood, injury, inoculation fears). The DSM-5 divides these specific phobias into five groups by the source of the fear: 1) blood, injuries and injections 2) situational fears 3) animals 4) natural environment and 5) other phobias. There is a high comorbidity rate within each category. Different cultures bring along different clinical phobias, with 'fear-relevance' being determined by specific culture factors. This is the opposite of the biological view, which holds that there are universally feared stimuli and events created through evolution.

What is the aetiology of Specific Phobias?

A common debate is whether phobias are learned or acquired through evolution. A view held today is that different ways of acquisition go with different phobias. Phobias under the psychoanalytic view are defenses against anxiety coming from id impulses that were repressed. This is a way of avoiding confrontation with the real conflict. Symbolic interpretation of case histories in psychoanalysis can serve as a source of insight.

The popular study of “Little Albert” (1920) still stands today as an example of classical conditioning as an explanation for phobia. Yet, criticism of the classical conditioning explanation is:

• While the classical conditioning approach says traumatic experiences are necessary for conditioning, some phobics cannot remember such an event at the point when they acquired their fear.
• Even if an individual experiences a traumatic event, it does not necessarily mean that a phobia will be acquired.
• Phobias are usually limited to a specific group of stimuli, even though in the simple conditioning model all stimuli should be equally likely conditioned. Also, stimuli that pose a danger that did not exist before, such as an electricity outlet, are less likely to be associated with aversion or danger, even though they pose a potential source of danger as well.
• The clinical phenomenon of incubation cannot be applied to the simple conditioning model. Instead of growing fear with more and more encounters of the stimuli, the conditioning model postulates that extinction should rather occur.
• At least some phobias can be explained by the occurrence of traumatic conditioning experiences, but not all.

People acquire phobias of life-threatening stimuli that have always existed, but rarely of stimuli that pose a danger that have only recently evolved. The first theory by Seligman called biological preparedness proposes that if we avoid stimuli that have been dangerous to our ancestors, we will have a greater chance of surviving. An experiment showed that people are more easily conditioned with a picture of a fearful stimulus together with an electric shock than if it is a picture of a non-fearful stimulus and are more resistant to extinction. The second theory by Poulton and Menzies argues that adult phobias can be explained by a failure of normal habituation, which usually occurs in childhood when children are first frightened of a stimulus but after several exposures the fear disappears. The evolutionary account is not easy to verify, because of possible post-hoc construction of evolutionary explanations. According to the adaptive fallacy any stimulus can be explained by coming up with a threatening consequence for it.

With functional neuroimaging techniques, we can look at specific brain regions playing a role in specific phobias. The key structure mediating fear responses to phobic stimuli is the amygdala. It is involved in forming and storing memories associated with emotionally relevant events. It coordinates this with info from subcortical nuclei and higher cortical areas and then relays feedback to the thalamus, which coordinates motor responses. It has also been seen that BII phobia and dental phobia are different in the way that they affect the brain, since it can result in a decrease of parasympathetic response resulting in fainting.

Phobias are acquired in different ways depending on the type of phobia. Not all phobias are acquired through the occurrence of a traumatic event and might be acquired over long-term and gradual experiences that the individual is not always aware of (mostly in animal and height and water phobias). There is evidence that disgust, a food-rejection emotion, plays a role in small animal phobias and blood-injury-injection phobia. The disease-avoidance model states that an individual with high level of disgust sensitivity is more prone to acquiring an animal phobia. Also, there is evidence for a link between specific phobias and panic and panic disorder. Comorbidity rates lie between 40 and 65%, meaning that people with specific phobias also often suffer from panic, especially those with situational phobias. Claustrophobia and height phobia have close links to panic disorder, because sufferers also hold anxiety expectations and focus on bodily sensations. In height phobia ambiguous bodily sensations are experienced as threatening, which is common in panic disorder.

How can Specific Phobias be treated?

Exposure therapy offers an individual suffering from a specific phobia to overcome their dysfunctional beliefs by experiencing that they do not take place when exposed to the feared stimuli. This form of therapy together with cognitive therapy techniques can yield results in just a 3-hour session.

What is a Social Anxiety Disorder and what is the prevalence?

Individuals experiencing social anxiety disorder fear social situations and try to avoid these because they are afraid of negative evaluation or that they will embarrass themselves. Sufferers may also experience problems with depression and substance abuse. The lifetime prevalence rate lies between 4 and 13% (for western societies), with females being affected more than males. Onset is in the early to mid-teens, usually before turning 18. From all main anxiety disorders, it has the lowest remission rate. There are cultural differences in prevalence rates, with Southeast Asian countries showing lower rates than Western countries.

What is the aetiology of Social Anxiety Disorder?

Social anxiety disorder is not put in the same category as simple phobias in DSM-5 because social anxiety is central to the aetiology of social anxiety disorder and information processing and interpretation biases are involved. Social anxiety disorder can be compared to generalized anxiety disorder (GAD) in its prevalence as being the most common anxiety disorder.

There is more and more evidence that genetics might reflect a component of social anxiety disorder. Twins’ studies reveal moderate genetic influence and parents with social anxiety disorder often times have children with social anxiety disorder. Submissiveness, anxiousness, social avoidance, and behavioral inhibition (where children seem quiet and isolated) seem to have a genetic component in social anxiety disorder. A different account proposes that social anxiety disorder shares genetic components with other anxiety disorders. Yet, the possibility is proposed that there is an inherited and unique element specific to social anxiety disorder that makes up 13% of the variance in social fears. There is evidence that children that have an inhibited temperament style are more likely to acquire social anxiety disorder. Because social anxiety disorder occurs at such an early age in comparison to most main anxiety disorders, there is the argument that developmental factors contribute to the acquisition of social anxiety disorder. Individuals suffering from social anxiety disorder have parents that control them more, discipline them using shame as a tool, are in general colder and do not socialize as much. If those are actual causal factors cannot be said at the moment. Sufferers of social anxiety disorder believe more than any other group of sufferers of anxiety disorders that a negative social event will occur, which makes them avoid social situations. Also, they are more critical when judging their own performance and do not process positive social feedback as easily. This supports the maintenance of dysfunctional beliefs that a social phobic hold. When self-focused attention occurs during a social performance, a social phobic directs attention onto himself and his anxiety, and this leads to their belief that people can see how anxious they feel inside. They take on an observer's perspective rather than a personal perspective. This is known as self-focused attention, which in a way acts as a distractor from the actual task and prevents the individual from best performance. After a social event, a social phobic engages in post-event rumination in which critical self-evaluation is practiced.

How can Social Anxiety Disorder be treated?

An effective way of treating social anxiety disorder can occur by administering cognitive behavior therapy and pharmacological treatment. CBT treatments that are effective include:

• Exposure therapy, in vivo or with the therapist playing a stranger.
• Social skill training with modelling, behavioral rehearsal, corrective feedback and positive reinforcement.
• Cognitive restructuring, challenging dysfunctional beliefs and reducing self-focused attention.

The best approach is combining pharmacological treatment (MAOIs, SSRIs, benzodiazepines and beta-adrenergic blockers have all been found to be effective) with cognitive-behavioural therapy, with the former providing immediate gains and the latter ensuring long-term effectiveness.

What is panic disorder and agoraphobia and what is the prevalence of these disorders?

In panic disorder a person repeatedly experiences panic or anxiety attacks. They are accompanied by physical symptoms that occur in great variety (e.g., dizziness, nausea, heart palpitations). Many will experience a feeling of terror or depersonalization, a feeling of being disconnected from one's body or surrounding. The diagnosis of panic disorder is made when the attacks occur repeatedly and unexpectedly, and when the individual suffers from at least one month of concerns of experiencing another attack. Panic attacks may either occur through association with a specific situation or they occur unpredictably. In an attack a peak is reached within 10 minutes consisting of intense fear and the development of a number of symptoms. Panic disorder often occurs together with agoraphobia, because the person tries to avoid unsafe, public places where an attack could occur, and therefore they often stay home. Agoraphobia is a separate diagnosis represented in the DSM-5 and is characterized by feelings of fear and/or anxiety of a place where the individual feels either trapped or unsafe, with a strong urge to return to a safe place like home. Sufferers often do not leave the house, or only rarely with trusted friends and family. Due to this fear of leaving their safe place, they become severely disabled in daily life and often have to rely on others to assist them with basic tasks like grocery-shopping.

Onset occurs in early adulthood or in adolescence, often after a stressful life period. Prevalence rates lie between 1.5 to 3% for panic disorder and 0.4 to 3% for agoraphobia, with women suffering more often from either of them. There is a cultural difference in manifestation and variance in prevalence of the disorder. In Western cultures individuals deal with panic disorder by employing avoidance and withdrawal strategies, while Latinos show their distress in an external form (e.g., screaming).

What is the aetiology of Agoraphobia and Panic Disorder?

Biological factors were often a focus in finding causes for panic disorder, but now it has become acknowledged that psychological and cognitive factors also contribute to the aetiology and maintenance. Because agoraphobia only recently become a distinct disorder in the new DSM-5, not much research has been spent on its aetiology. Therefore, the following theories are focused on panic disorder.

Hyperventilation plays a central role in panic attacks. Through the rapid breathing, the blood pH level is raised, and body cells receive less oxygen, which in turn produces cardiovascular changes that ultimately create symptoms of panic attacks. These symptoms are recognized by the individual as anxiety. Evidence for this comes from biological challenge tests that artificially create panic attacks. Suffocation alarm theories propose that increased CO2 intake may activate an alarm system that is overly sensitive to suffocation and therefore produces the typical anxiety of a panic attack. More than patients of other anxiety disorders, patients of panic disorder often report problems with a feeling of suffocation and shortness of breath during phases of anxiousness. Yet, when told to hold their breath, they do not experience more anxiety than control subjects, meaning a more sensitive suffocation alarm system is not present. Interpretation of the physiological changes seems to be a critical point of the causal factor in panic disorder, as induced symptoms only create a full panic attack for individuals that have suffered from repeated panic attacks before.

Norepinephrine plays a role in the aetiology of panic disorder. The proposition of overactivity in the noradrenergic neurotransmitter system holds that there is a deficiency of gamma-aminobutyric (GABA) neurons in patients with panic disorder and GABA neurons have the task of inhibiting noradrenergic activity.

Goldstein and Chambless (1978) have worked with the classical conditioning approach, according to which a predictor of a panic attack is the internal conditioned stimulus (CS), established by the experienced internal cue (e.g., dizziness). Bouton, Mineka, and Barlow argue that anxiety precedes an attack, which is the learned reaction (CR) to detected cues (CS), and that panic is a way of handling the existing trauma.

Anxiety sensitivity explains that sufferers of panic disorder acquire a set of beliefs that symptoms will bring about consequences that will cause them harm, which in turn leads them to fear anxiety symptoms. Non-clinical controls or individuals with different anxiety disorders score significantly lower on the Anxiety Sensitivity Index than individuals with panic disorder.

Often times bodily sensations are ambiguous and panic disorder sufferers interpret these sensations directly as threating, making it a catastrophic misinterpretation of bodily sensations. This causes the anxiety which leads to a panic attack. Individuals with panic disorder pay more attention to bodily sensations. The expectancy of the attack is critical, as when participants were given compressed air, which they were told was CO2, they had a panic attack, nevertheless. Hence, there is a cognitive bias in the interpretation of and reaction to bodily symptoms.

Even though some sufferers experience many panic attacks, they often do not seem to realize that the feared outcome never happens. This happens because of developed safety behaviors, which are certain behaviors that are automatically done by sufferers when they believe they are having a panic attack. This automatic behavior is then thought of to be the reason why some catastrophic outcome didn't occur, therefore they continue doing it every time, resulting in the maintenance of anxiety. Because of this big role they play in the maintenance of anxiety in panic, it is one of the key behaviors that should be modified attacks or eliminated in therapies.

How can a panic disorder be treated?

Effective treatments include psychoactive medication (usually as first line treatment), tricyclic antidepressants and benzodiazepines, structured exposure therapy, and cognitive behavior therapy (CBT). In exposure therapy, the bodily experiences that precipitate a panic attack are induced and physical and cognitive techniques can be used to deal with the symptoms of panic in a safe condition. Cognitive therapy aims to achieve success by having the individual learn through information and experiences that their beliefs are dysfunctional and that their responding is faulty. A program would include educating the individual about the nature and physiology of panic attacks, breathing training for controlling hyperventilation, cognitive restructuring therapy, interoceptive exposure, and the prevention of safety behaviours.

What is a Generalized Anxiety Disorder (GAD)?

People with generalized anxiety disorder consistently worry about future events due to the anxiety they experience in regard to them. Worrying is no longer experienced as a normal reaction to some events but becomes chronic and is directed to issues that other people would not even consider a threat. The individual feels their worrying is not under control, neither being able to control beginning nor end of a bout of worry. They also engage in catastrophizing (magnification) of worries and the problem does not seem to get better, but rather worse through the continuous worrying. Physical symptoms such as fatigue, muscle tension, nausea, headache and trembling may also be present. A diagnosis of GAD based on the DSM-5 can be made if the person exhibits:

• Unreasonable much fear or anxiety relating to multiple areas such as health, finance, family, work, school
• Fear relating to at least two of the above-mentioned areas and accompanying severe anxiety lasting for at least three months
• Restlessness, agitation or muscle tension is seen besides anxiety
• Behaviors such as frequent reassurance seeking, avoiding areas of activity relating to anxiety, and procrastination or excess effort preparing activities are also seen as a result of the anxiety

There is a high comorbidity rate with other anxiety disorders and depression and there are double as many women suffering from GAD as men. The lifetime prevalence rate of GAD is more than 5%. GAD is also associated with a significant impairment in the sufferer's psychosocial functioning, role functioning, health-related quality of life and work productivity.

What is the aetiology of Generalized Anxiety Disorder (GAD)?

There is the suggestion that there is an inherited component in GAD. Yet, because of only modest evidence of a specific genetic component, most focus is on the psychological and cognitive accounts. However, some recent neuroimaging studies have shown that the prefrontal brain areas are implicated in extreme worry, and that some areas important in emotional regulation seem to be less active, suggesting that a diminished capacity for emotional regulation could be associated with GAD.

There is experimental evidence that sufferers of GAD pay more attention to threatening stimuli and information, with information processing biases supporting the maintenance of bouts of worries and perceived threats. Anxious individuals also show a threat-interpretation bias, meaning that they interpret ambiguous stimuli more often as threatening or negative. Attention is pre-attentionally directed to threatening stimuli, to verbal stimuli and pictures of threatening emotional faces. Opposing to that, people that are not anxious deliberately avoid attending to threatening stimuli. Information processing biases may be the cause for experienced anxiety. Evidence from studies inducing information processing biases show that this leads to changes in state anxiety and to threatening interpretation of new stimuli. It was thought that anxiety causes threat-interpretation biases, but it seems to be the other way around, learned threat-interpretation biases result in elevated levels of anxiety. Therefore, attention bias modification (ABM) was created, which is a treatment where biases are reversed.

Individuals with GAD hold the dysfunctional belief that by worrying they can prevent future catastrophes, which motivates them to continue worrying. Another account holds that this chronic worrying takes the function of a distractor from other negative emotions or phobic images that are even more stressful. This can be supported by the evidence that little physiological or emotional arousal is produced by worrying. Another theory focuses on metacognitions, which are overarching processes responsible for our thinking. Metacognitions are responsible for adaptive thoughts of worry in order to anticipate and avoid problems and if they occur, find solutions. However, sufferers from GAD have developed beliefs about worrying which makes it distressing on one hand, but they also find worrying positive as it helps them avoid and solve problems.

Worriers do not tolerate uncertainty; they are perfectionists and feel responsible for negative outcomes. The individual tries to resolve the problems, but this gets hindered through feelings of doubt to successfully solve the problem.

How can a Generalized Anxiety Disorder (GAD) be treated?

A crucial point is deciding which treatment works best for successful therapy outcomes of GAD. Psychological therapies, such as CBT or self-help programs are usually the best option for a long-term treatment success, but if the patient experiences suicidal intentions or other extreme stress, medication can be used for first management of the problem. Also, it should be considered what approach is effective at what point in treatment, regarding symptom severity and what the client prefers.

Anxiolytics such as benzodiazepines are often thought of as the best prescribed drug for anxiety GAD. However, more than 50% are prescribed antidepressants (SSRIs or SSNIs) as they have been proven effective, and 'only' 35% are prescribed benzodiazepines. The use of antidepressants makes sense because they are better tolerated by patients, and anxiety is often comorbid with depression.

Psychological treatments are developed out of behavioral and cognitive methodologies, and an example is stimulus control treatment, which works by helping the client minimize the contexts in which they can worry, such as only at a certain time of day or in a specific location.

These elements are included in CBT to provide relief from cognitive biases and dysfunctional beliefs:

• Self-monitoring: clients become aware that they cognitively construct future events and that these are not real and hence will most likely not occur
• Relaxation training: these types of techniques, such as progressive muscular relaxation, yield the same effects as some forms of cognitive therapy
• Cognitive structuring: dysfunctional thoughts and biases are challenged and replaced with more accurate thoughts. Achieving this can be aided by the use of an outcome diary. Another form is metacognitive therapy, where metacognitive beliefs are challenged
• Behavioral rehearsal: coping strategies are applied when a worry is triggered. This can be done through imagined or actual rehearsal

What is obsessive compulsive disorder?

An individual suffering from obsessive-compulsive disorder (OCD) experiences obsessions and compulsions, the former being known by intrusive and recurring thoughts and the latter by repetitive or ritualized behavior patterns. The thoughts are seen as uncontrollable by the individual and he or she engages in rituals to prevent a negative outcome. The ritualized behavior is also seen as a way to reduce stress and anxiety. This can take place in the form of repetitive behaviours (e.g., hand washing, checking) or mental acts (e.g., counting, repeating words mentally). The sufferer knows that these excessive compulsions are irrational and experiences the obsessions and compulsions as unpleasant. Common obsessions are fear of contamination, unwanted sex, thoughts about harm, and fear of accidents.

Lifetime prevalence of OCD is about 2.5%, with more women being affected. OCD is characterized by onset in early adulthood or early adolescence. This is true regardless of cultural background, with the exception of more religious and aggressive obsessions being present in Brazilians and Middle Easterners. OCD is now a separate chapter in the DSM-5, and the criteria for it are:

• Presence of obsessions like unwanted and repeated thoughts, urges or images which the individual wants to ignore and/or
• Experiencing compulsions compelling the sufferer to carry out and repeat certain behaviours or mental activities
• The sufferer believes that these actions must be carried out in order to prevent some sort of catastrophic outcome, which is illogical and has no connection to the behaviour
• Compulsions and obsessions cause difficulty in a person's life and consume one hour or more of a person's day

What are other OCD-related disorders?

Other OCD-related disorders include body dysmorphic disorder (BDD), hoarding disorder, hair-pulling disorder, and skin-picking disorder. Body dysmorphic disorder refers to an obsession with ones perceived flaws or defects in their physical appearance. Hoarding disorder refers to a sufferer's difficulty discarding possessions resulting in a living area severely congested by clutter. Hair-pulling disorder (trichotillomania): refers to the compulsive act of pulling out one's own hair. Lastly, skin picking disorder: recurrent picking of the skin resulting in skin lesions.

What is the aetiology of obsessive-compulsive disorder?

OCD can begin after a traumatic brain injury, creating a neurophysiological deficit that produces the 'doubting' characteristic of OCD. The frontal lobes and basal ganglia seem to play a role in this. Another account of 'doubting' holds that basic information processing and executive functioning are impaired in sufferers of OCD, alongside with spatial working memory, spatial recognition, visual attention, visual memory, and motor response inhibition deficits. There is also the argumentation that compulsions are produced from genetically stored and learned behaviors that cannot be inhibited by the brain, mostly involving the inhibitory pathways projecting via basal ganglia.

With 'doubting' being a main component in OCD, it is suggested that OCD might involve a general memory deficit, and also less confidence from the client's side that the memory reviewed is correct and whether a memory was real or imagined. However, recent evidence shows that doubting in OCD may not be due to a deficit in memory, but due to a general deficit in executive functioning instead. It is also consistent with much evidence showing that the lack of confidence in one’s recall is a consequence of the compulsive checking, so the more one checks, the less confident they end up being about what they checked.

Clinical constructs are constructs that describe a combination of thoughts, beliefs, cognitive processes, and symptoms that are seen in psychopathology. These constructs are then observed to see how symptoms are affected by cognitive factors. Three constructs now looked at are inflated responsibility, thought-action fusion, and mental contamination.

A main feature of OCD is that sufferers feel that they hold responsibility for the content of their thought. They also believe that there are potentially harmful consequences to their obsessional thoughts. Another dysfunctional belief is that of inflated responsibility, which means an individual believes he can prevent harm and that it is his or her responsibility to make sure that this negative outcome does not occur. In an experiment, inflated responsibility was induced, which subsequently caused an elevated amount of compulsive checking. Believing that one's thoughts are like actually performing them or that one's thoughts will come true, is known as thought-action fusion. It is commonly seen in OCD and is best described as thinking that one's thoughts can (in some way) directly affect whatever happens in the world. If the believed action is negative, trying to suppress the thought and action can be quite effortful, causing significant distress in the person.

Feelings of 'dirtiness' caused without any physical touch can be provoked by thoughts of specific images or memories, or they can be provoked by emotional experiences like humiliation, betrayal or degradation. These thoughts cause mental contamination and can be a reason why one has to compulsively wash themselves. Individuals with OCD engage in thought suppression if they encounter an intrusive thought. The 'rebound effect' says that suppressing thoughts will make them come back in greater frequency once suppression is stopped. Suppression of intruding thoughts creates a negative emotional state which becomes associated with the intruding thought. Experiencing this negative emotion at some other point in time will then elicit the intrusive thought.

In OCD a critical feature is that of perseveration, meaning an individual with OCD engages in longer perseveration of an activity than non-OCD sufferers. They themselves recognize it as excessive and unpleasant. The mood-as-input hypothesis explains that the current mood is a way of measuring whether a task was completed with success or not. Regarding the nature of OCD, the sufferer feels a strong negative and anxious mood during the task, which leads him or her to feel that they never successfully completed it. The 'stop-rule' says one must continue until the task is completed successfully, which is perpetuated by the inflated responsibility. Inflated responsibility has to occur with negative mood together though so an individual will persevere at a compulsive activity.

How can OCD be treated?

The most effective treatment is exposure and ritual prevention (ERP), which consists of two components. The first component aims at graded exposure to what elicits the distress. In the second component, the goal is to prevent the client from following their rituals, by which anxiety is extinguished and dysfunctional beliefs are disconfirmed. When rituals are abolished, anxiety is not negatively reinforced anymore. Long-term effectiveness of the treatment lies at 75% and it is flexible in its application.

What is cognitive behaviour therapy (CBT)?

There is a 30% drop out rate in exposure and ritual prevention (ERP) due to the fear of exposure to what triggers OCD in the individual. In CBT, the dysfunctional beliefs such as responsibility appraisal, the over-importance of thoughts, and exaggerated perception of threat are challenged.

What are pharmacological and Neurosurgical Treatments?

Even though pharmacological treatments, usually serotonin and SSRIs, are effective, they have a high relapse rate when medication is not continued. Tricyclic antidepressants are effective if OCD occurs together with depression. Psychological treatment such as ERP has equally good short-term effects as drug treatment, does not produce side effects and yields better results in the long-term. Neurosurgery such as cingulatomy is a last resort treatment when all other approaches have failed.

What is a Post-Traumatic Stress Disorder (PTSD) and Acute Stress Disorder (ASD)?

In post-traumatic stress disorder (PTSD) a causal factor for the symptoms is the identification of exposure to a specific fear-evoking event. PTSD is caused by symptoms that follow a fear-evoking traumatic event (e.g., war, rape, abuse). The symptoms are grouped in three categories: increased arousal and reactivity, avoidance responding, negative changes in mood & cognition and intrusive symptoms. In the DSM-5, severe (but not life-threatening) stress has been added under the possible causal factors in PTSD, which sparked controversy due to facilitating the faking of symptoms. The diagnostic criteria are:

• Death or threatening death is experienced to oneself or is being witnessed
• Flashbacks or intrusive images or thoughts of the traumatic event are re-experienced.
• Stimuli that are associated with the trauma are avoided
• Two or more changes to mood and/or thought processes (e.g., feeling disconnected, reduced interests, inability to remember moments of the traumatic event)
• Constant experiencing of symptoms for over a month such as increased arousal, with sleep difficulty, anger outbursts, concentration difficulties, hypervigilance and startle response. This causes the individual to be impaired in occupational or social functioning
• Symptoms worsened or started after the traumatic event and last for at least a month

At least between 1 and 3% of people experience PTSD at one point in their lifetime, with women being more vulnerable to developing PTSD and culture differences existing between Caucasian disaster victims and Latinos or African Americans.

Acute stress disorder (ASD) is very similar to PTSD but characterized by a shorter duration (3 days to a month). The symptoms exhibited are basically the same of PTSD. There is debate whether or not ASD is a disorder or just a normal way of reacting to some disturbing events. ASD is also seen as a potential precursor for PTSD by some, whether this is true is not yet determined.

What is the aetiology of PTSD?

There are five main theories which aim to explain PTSD, all concentrating on different features of the disorder: avoidance and dissociation, conditioning theory, emotional processing theory, 'mental defeat', and dual representation theory.

Studies have led to finding a genetic element to PTSD, and the heritability component has been estimated to be 30%. Therefore, it has been suggested that PTSD develops from an interaction between a biological vulnerability and an extreme traumatic experience. Some biological causes for a vulnerability to PTSD are speculated to be:

• An underdeveloped hippocampus (of which it is known to be critical in relating memories to emotions)
• Failure of areas like the ventromedial frontal cortex in controlling fear centers such as the amygdala
• Heightened startle responses due to genetics, and fear-related hormonal secretion

Since not all people develop PTSD following a life-threatening event, some individuals must be vulnerable to developing it. Factors that contribute to this include feelings of responsibility for the traumatic event, having experienced instability in the family life, history of PTSD in the family, higher levels of anxiety or suffering from another psychological disorder. People with high intelligence are a lot more resistant to PTSD than people of low intelligence, which can be led back to the ability to develop coping strategies. Also, the experiences which are reported by the victims indicate how information about the trauma was processed and stored.

Individuals exhibiting avoidance or dissociation coping strategies are more likely to develop PTSD. Avoidance coping strategies are seen in individuals who actively try not to think about their trauma. Feeling detached from one's mind and body is known as dissociation, and if an individual experiences this coping strategy right before or during a traumatic experience, they are known to be of higher risk for developing PTSD.

The conditioning theory works with the explanation of classical conditioning, saying that when individuals encounter cues that were associated with place and time of the trauma, they trigger the same experience as that of the trauma.

A PTSD sufferer will avoid contexts that will trigger associations to the trauma. It becomes difficult for cues associated with the trauma to be associated with positive associations again. Because the event holds such a strong significance, the associations formed are unlike those from everyday experiences. This is called the emotional processing theory.

If an individual adopts the mental defeat view, then they take on the role of feeling like a victim and see the world as negative and also recall the trauma according to those feelings and views. Maladaptive behaviors and cognitive strategies may be adopted that support the maintenance of PTSD. An account by Ehlers and Clark holds that the sufferers do not see the event as part of their life, because they feel they are not in control over it. They feel as if they cannot change the course of their life anymore and that the traumatic event has changed it in a permanent way.

In the dual representation theory, there are two separate memory systems, the verbally accessible memory (VAM) system and situationally accessible memory (SAM) system, the former recording conscious memories from the time of the trauma and the latter registering information that was not consciously recognized because it occurred too brief. The SAM system hence stores sensory and response information. Evidence supports this theory, both systems being linked to the amygdala and findings showing that PTSD sufferers explain the flashback periods in an elaborate and detailed way, frequently mentioning death, horror, fear, and helplessness.

How can PTSD be treated?

Treating PTSD has two aims. Preventing the development of PTSD and if this is (partly) unsuccessful because symptoms do appear, treatment of the symptoms. If the latter is the case, most treatments rely on some form of exposure like flooding, EMDR and cognitive restructuring.

In order to prevent an individual from developing PTSD after a traumatic life event, there has been an established intervention called psychological debriefing, or immediate and rapid debriefing, which is administered within 24-72 hours of the occurrence of the event. Techniques such as critical incident stress management are used where the individual can express his feelings and experiences, is reminded that he is a normal person that had to experience such an event and can learn coping strategies. Yet, psychological debriefing does not separate people that would not develop PTSD in the first place from those that would and that need long-term support. Also, there is lacking evidence of the effectiveness of rapid debriefing.

The extinction of associations between trauma cues and fear responses and the disconfirmation of dysfunctional beliefs is aim of the effective exposure therapy. Exposure is achieved by the client depicting the situation in a written narrative or with computer-generated imagery. Imaginal flooding is a further technique in which the client is supposed to visualize the traumatic event for a long period of time. This is often paired with graded in vivo exposure. Exposure therapies are more effective than medication and social support, as studies show. In another critically judged form of PTSD treatment, called eye-movement desensitization and reprocessing (EMDR), the client follows the therapist's finger, moving backwards and forwards, while concentrating on a traumatic image or memory. The fearful images are thereby reconstructed and deconditioned.

In cognitive restructuring the aim is to change the individual's dysfunctional beliefs about the world and themselves, acquired from the trauma, and exchanging negative or intrusive thoughts. Foa and Rothbaum suggest that the two dysfunctional beliefs an individual with PTSD holds are: “The world is a dangerous place” and “I am totally incompetent”. Chronic PTSD is the result of avoiding situations which could disprove the dysfunctional beliefs. While exposure therapy disconfirms these beliefs, cognitive therapy aims to change PTSD-related cognitions, but findings show that a therapy combining these two approaches does not achieve changes in dysfunctional cognitions.