The phobia typically results in a rapid onset of fear and is present for more than six months. The affected person goes to great lengths to avoid the situation or object, to a degree greater than the actual danger posed. If the feared object or situation cannot be avoided, the affected person experiences significant distress. With blood or injury phobia, fainting may occur. Agoraphobia is often associated with panic attacks. Usually, a person has phobias to a number of objects or situations.
Phobias can be divided into specific phobias, social phobia, and agoraphobia. Types of specific phobias include those to certain animals, natural environment situations, blood or injury, and specific situations. The most common are fear of spiders, fear of snakes, and fear of heights. Occasionally they are triggered by a negative experience with the object or situation. Social phobia is when the situation is feared as the person is worried about others judging them. Agoraphobia is when fear of a situation occurs because it is felt that escape would not be possible.
It is recommended that specific phobias be treated with exposure therapy where the person is introduced to the situation or object in question until the fear resolves. Medications are not useful in this type of phobia. Social phobia and agoraphobia are often treated with some combination of counselling and medication. Medications used include antidepressants, benzodiazepines, or beta-blockers.
Specific phobias affect about 6–8% of people in the Western world and 2–4% of people in Asia, Africa, and Latin America in a given year. Social phobia affects about 7% of people in the United States and 0.5–2.5% of people in the rest of the world. Agoraphobia affects about 1.7% of people. Women are affected twice as often as men. Typically the onset is around the age of 10 to 17. Rates become lower as people get older. People with phobias are at a higher risk of suicide.
Beneath the lateral fissure in the cerebral cortex, the insula, or insular cortex, of the brain has been identified as part of the limbic system, along with cingulated gyrus, hippocampus, corpus callosum and other nearby cortices. This system has been found to play a role in emotion processing and the insula, in particular, may contribute through its role in maintaining autonomic functions. Studies by Critchley et al. indicate the insula as being involved in the experience of emotion by detecting and interpreting threatening stimuli. Similar studies involved in monitoring the activity of the insula show a correlation between increased insular activation and anxiety.
In the frontal lobes, other cortices involved with phobia and fear are the anterior cingulate cortex and the medial prefrontal cortex. In the processing of emotional stimuli, studies on phobic reactions to facial expressions have indicated that these areas are involved in processing and responding to negative stimuli. The ventromedial prefrontal cortex has been said to influence the amygdala by monitoring its reaction to emotional stimuli or even fearful memories. Most specifically, the medial prefrontal cortex is active during extinction of fear and is responsible for long-term extinction. Stimulation of this area decreases conditioned fear responses, so its role may be in inhibiting the amygdala and its reaction to fearful stimuli.The hippocampus is a horseshoe-shaped structure that plays an important part in the brain’s limbic system because of its role in forming memories and connecting them with emotions and the senses. When dealing with fear, the hippocampus receives impulses from the amygdala that allow it to connect the fear with a certain sense, such as a smell or sound.
The amygdala is an almond-shaped mass of nuclei that is located deep in the brain’s medial temporal lobe. It processes the events associated with fear and is linked to social phobia and other anxiety disorders. The amygdala's ability to respond to fearful stimuli occurs through the process of fear conditioning. Similar to classical conditioning, the amygdala learns to associate a conditioned stimulus with a negative or avoidant stimulus, creating a conditioned fear response that is often seen in phobic individuals. In this way, the amygdala is responsible for not only recognizing certain stimuli or cues as dangerous but plays a role in the storage of threatening stimuli to memory. The basolateral nuclei (or basolateral amygdala) and the hippocampus interact with the amygdala in the storage of memory, which suggests why memories are often remembered more vividly if they have emotional significance. In addition to memory, the amygdala also triggers the secretion of hormones that affect fear and aggression. When the fear or aggression response is initiated, the amygdala releases hormones into the body to put the human body into an "alert" state, which prepares the individual to move, run, fight, etc. This defensive "alert" state and response are known as the fight-or-flight response. Inside the brain, however, this stress response can be observed in the hypothalamic-pituitary-adrenal axis (HPA). This circuit incorporates the process of receiving stimuli, interpreting it and releasing certain hormones into the bloodstream. The parvocellular neurosecretory neurons of the hypothalamus release corticotropin-releasing hormone (CRH), which is sent to the anterior pituitary. Here the pituitary releases adrenocorticotropic hormone (ACTH), which ultimately stimulates the release of cortisol. In relation to anxiety, the amygdala is responsible for activating this circuit, while the hippocampus is responsible for suppressing it. Glucocorticoid receptors in the hippocampus monitor the amount of cortisol in the system and through negative feedback can tell the hypothalamus to stop releasing CRH.
Studies on mice engineered to have high concentrations of CRH showed higher levels of anxiety, while those engineered to have no or low amounts of CRH receptors were less anxious. In phobic patients, therefore, high amounts of cortisol may be present, or alternatively, there may be low levels of glucocorticoid receptors or even serotonin (5-HT).
Disruption by damage
For the areas in the brain involved in emotion—most specifically fear— the processing and response to emotional stimuli can be significantly altered when one of these regions becomes lesioned or damaged. Damage to the cortical areas involved in the limbic system such as the cingulate cortex or frontal lobes have resulted in extreme changes in emotion. Other types of damage include
Klüver–Bucy syndrome and Urbach–Wiethe disease. In Klüver–Bucy syndrome, a temporal lobectomy, or removal of the temporal lobes, results in changes involving fear and aggression. Specifically, the removal of these lobes results in decreased fear, confirming its role in fear recognition and response. Bilateral damage to the medial temporal lobes, which is known as Urbach–Wiethe disease, exhibits similar symptoms of decreased fear and aggression, but also an inability to recognize emotional expressions, especially angry or fearful faces.
The amygdala’s role in learned fear includes interactions with other brain regions in the neural circuit of fear. While lesions in the amygdala can inhibit its ability to recognize fearful stimuli, other areas such as the ventromedial prefrontal cortex and the basolateral nuclei of the amygdala can affect the region's ability to not only become conditioned to fearful stimuli, but to eventually extinguish them. The basolateral nuclei, through receiving stimulus info, undergo synaptic changes that allow the amygdala to develop a conditioned response to fearful stimuli. Lesions in this area, therefore, have been shown to disrupt the acquisition of learned responses to fear. Likewise, lesions in the ventromedial prefrontal cortex (the area responsible for monitoring the amygdala) have been shown to not only slow down the speed of extinguishing a learned fear response, but also how effective or strong the extinction is. This suggests there is a pathway or circuit among the amygdala and nearby cortical areas that process emotional stimuli and influence emotional expression, all of which can be disrupted when an area becomes damaged.