Etiology
Intense anxiety or unexpected panic responses in the presence of specific objects or situations can mark phobia onset, but this is not necessarily the only causal route to phobic acquisition.[14] Disgust, either alone or in combination with fear, may be involved in the onset and maintenance of various animal (e.g., spiders, snakes, worms) and blood-injection-injury phobias.[15] Onset can also occur through indirect means, such as observing others reacting fearfully or receiving negative information.[14] However, a past event or specific reason for the onset of a phobia is not always possible to identify.
Some phobias (e.g., animal phobias) may arise solely due to the evolutionary threat relevance of their stimuli.[16] Familial concordance rates among first-degree biological relatives tend to be moderate. Heritability studies suggest that animal and blood-injection-injury phobias have the greatest heritability indices, of roughly 32% and 33%, respectively; however, there is limited research in this area.[17]
Pathophysiology
Amygdala, anterior cingulate cortex, and insula hyperactivity is believed to be the underlying mechanism of action. This theory is based on research noting significant reductions in site-specific neural activity in these areas following evidence-based exposure treatments.[18] Neuroimaging studies have also demonstrated increased amygdala activation upon exposure to phobic-relevant cues and heightened activity in the thalamic, insula, and dorsal anterior cingulate cortex regions.[18][19][20][21][22] Meta-analyses suggest that the left amygdala/globus pallidus, left insula, right thalamus, and cerebellum regions are all more active among phobics compared with non-phobic controls when exposed to phobic-relevant stimuli; exposure-based therapy leads to deactivation in the right frontal cortex, limbic cortex, basal ganglia, and cerebellum, with increased activity in the thalamus.[23] Reduced substance P-neurokinin 1 receptor availability during threat exposure (specific to the right amygdala) has been observed in a small, mixed sample of phobic patients.[24]
Functional neuroimaging studies have identified specific neural substrate patterns that differentiate phobic disorders from other anxiety disorders, including unique patterns of activation that discriminate among the various phobia subtypes.[25]
Acute, exaggerated parasympathetic nervous system activity upon exposure to stimuli is thought to underlie the vasovagal syncope that occurs in up to 80% of people with blood-injection-injury phobia.[26][27]
Classification
Phobic stimuli[1]
Animal
Most commonly dogs, snakes, and insects.
Situational
Most commonly elevators, flying, and enclosed spaces (claustrophobia).
Natural environment
Most commonly storms, heights, and water.
Blood-injection-injury
Most commonly injections, blood draws, and medical procedures.
Other
For example, choking, vomiting, and clowns.
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