Blood-injection-injury type phobia

In a majority of specific phobias, affected individuals experience heightened anxiety when exposed to a phobic trigger.[2] While BII-phobics experience a similar reaction initially upon exposure, most ultimately respond to a trigger with a biphasic, or two-phase, fainting response.[3][6] In the first phase, phobics often experience an anxiety reaction characterized by elevated heart rate and heightened blood pressure, as occurs in most other phobias.[6] This is the result of increased activation of the sympathetic nervous system.[2] However, with BII phobia, a second phase usually follows closely, in which the phobic individual experiences a massive dip in heart rate and blood pressure[4][10] known as vasovagal response.[8] Stimulation of the vagus nerve, a part of the parasympathetic nervous system, is responsible for promoting the lowered heart rate and decreased blood pressure.[6] These physiological changes limit blood flow to the brain and can promote pre-syncope (lightheadedness, feelings of faintness) and syncope (fainting):[6] categorized in this instance as vasovagal fainting.[1] This second, fainting phase is not common to other phobias.[3]

A fainting response pattern is not seen in all individuals with BII phobia, but is found in a majority.[6] Up to 80% of those with BII phobia report either syncope or pre-syncope as a symptom when exposed to a trigger.[3]

Other symptoms that may evolve when exposed to phobic triggers include extreme chest discomfort, tunnel vision, becoming pale,[4] shock, vertigo, diaphoresis (profuse sweating), nausea, and in very rare cases asystole (cardiac arrest) and death.[3] Increase in stress hormone release (particularly of cortisol and corticotrophin) is typical.[3]

Neurological responses to phobic triggers include activation of the bilateral occipito-parietal cortex and the thalamus.[1] It has also been suggested that exposing a BII-phobic individual to a trigger will lead to decreased activity in the brain's medial prefrontal cortex (MPFC).[10] Diminished MPFC activity has been linked with impaired ability to control emotional responses. This lessened emotional control could contribute to a general lack of control over symptoms of anxiety arising when exposed to a phobic trigger.[10]

The cause of BII phobia is not yet well understood. Various studies indicate an underlying genetic cause, wherein certain genes make an individual more vulnerable to developing specific phobias. The contributing genes have not yet been identified.[1]

BII phobia has markedly strong familial aggregation — if present in a family, multiple members are likely to have the phobia.[1] This aggregation is stronger in BII phobia than in any other known phobic disorder:[2] upwards of 60% of those with the phobia have first-degree relatives who are also BII-phobics.[8] It is believed that this evidences the phobia's genetic underpinnings. One study estimated actual heritability of the phobia at 59%.[1]

Additionally, a majority of phobics attribute their fear to environmental factors. For instance, some sort of traumatic event involving blood, injury, or injection that conditioned them to fear those particular stimuli. Others self-report being conditioned by seeing another person react to the stimuli with a consistent pattern of fear.[1]

It has been theorized that exhibiting vasovagal response when exposed to blood was evolutionarily advantageous, and that this phobia is a vestige of an ancestral evolutionary mechanism.[8][9] Fainting may have acted as a form of tonic immobility,[8] allowing primitive humans to play dead in a situation where blood was being spilled, perhaps helping them to avoid the attention of enemies. It has also been suggested that the drop in blood pressure associated with seeing blood — as with an individual seeing blood from their own wound — occurs in order to minimize blood loss.[8][9]

Individuals typically seek therapeutic treatment for BII phobia in a bid to alleviate symptoms that arise when exposed to a phobic trigger. Therapists may use a combination of physical and psychological measures, such as cognitive-behavioral-therapy and applied tension (AT), in order to aid in extinguishing the individual's fear response.[6]

Early studies of methods to combat vasovagal fainting found that certain leg exercises and that individuals making themselves angry over imagined scenarios could increase blood pressure, thus elevating cerebral blood flow and preventing fainting upon exposure to a phobic trigger. A later study tested applied muscle tension as a way of preventing fainting when an individual with a fear of injuries was exposed to triggering visual stimuli. Lars-Göran Öst expanded upon this research, having BII-phobic individuals engage in applied muscle tension while shown blood stimuli. Those who were trained in the technique showed notable symptom improvement over the course of five one-hour treatment sessions.[8]

An AT treatment program most often involves an individual being instructed to clench their arm, leg, and chest muscles in 10 to 15 second intervals[6] as they are systematically exposed to triggers of increasing likeness to real blood or needles.[8] This program is designed to increase heart rate and blood pressure, counteracting vasovagal response.[8][6]

The method of applied tension remains popular — it is the most common BII phobia treatment suggestion, and has been found to be highly effective in a majority of BII-phobics. However, exposure-only cognitive-behavioral therapy (CBT) can also be effective, as can the method of applied relaxation (AR).[6]

CBT is a technique which promotes fear extinguishment by way of gradual, repeated exposure to feared stimuli. BII-phobics may be given pictures of needles or blood, asked to illustrate needles or scenes with blood, or to speak about their phobic triggers. This systematically progresses to the point of the individual directly confronting a phobic stimulus: being given a needle, witnessing blood being drawn, etc. As exposure continues, it is expected that the phobic response will become less pronounced, and symptoms less debilitating.[12]

While AT targets the phobia’s physiological response, aiming to raise blood pressure and directly prevent fainting, AR focuses mainly on helping an individual avoid the phobia’s associated anxiety. A phobic will learn progressive relaxation techniques to help to calm themselves upon exposure to a trigger.[6]

BII phobia is one of the more common types of phobia — it is estimated to affect about 3-4% of the general population.[3]

Onset of the phobia generally occurs in middle childhood, before the age of ten.[1] There are more reports of incidence of the phobia in younger individuals[4][1] and those with low education levels.[4] Some studies suggest that women also experience the phobia more frequently, however results are mixed concerning relative prevalences of the phobia between the sexes.[1]