____________________________________________________________________________ Anxiety Disorders
Specific Phobia Epidemiology
were diagnosed with SEPAD. Patients with panic disorder and SEPAD (versus no SEPAD) were more commonly female and younger and showed higher rates of childhood SEPAD and greater lifetime prevalence of mood disorder spectrum symptoms [63]. Risk Factors Children of adults with anxiety disorders have higher rates of anxiety disorders. Early, traumatic separation from attachment figures and a positive family history of anxiety or depressive disorders may also elevate risk of SEPAD, school phobia, and depressive-spectrum disorders during adolescence or adult- hood. Early, traumatic separation can include prolonged sever- ance of contact with the primary caregiver during the neonatal period; later sudden hospitalization; early loss of attachments from death or divorce; or an interactive pattern with an over- protective, needy, or depressed parent [64]. Clinical Course In one study, children with SEPAD were 3.5 times more likely to later develop panic disorder and more than twice as likely to develop any anxiety disorder but did not significantly differ in later development of depression or substance use disorder. These findings were considered supportive of a developmental psychopathology model of anxiety disorders [65].
Women are two to three times more likely than men to develop phobias, with the exception of blood-injection-injury phobia, which is evenly distributed by sex. Roughly 70% of individuals with specific phobia report more than one clinically relevant fear. Animals and heights are the most common stimuli, fol- lowed by flying, enclosed spaces, and blood-injection-injury. The average period of onset is 7 to 10 years of age, with declining probabilities of onset into later adulthood. Most animal phobias develop before 8 years of age [2; 41; 56]. The average age of treatment engagement is 31 years, although only 8% of persons with specific phobia are reported to seek treatment [56]. The odds of developing phobias are significantly less in His- panic and Asian individuals and greater in white individuals. Animal fears are prevalent in Japan and Hong Kong [56; 57]. Risk Factors For specific phobias, familial concordance rates among first- degree relatives are moderate. The greatest heritability indices are found in animal and blood-injection-injury phobias [58; 59; 60]. Intense anxiety or unexpected panic responses in the presence of specific objects or situations can mark phobia onset but are not the sole causal route. Disgust, either alone or combined with fear, may trigger the onset and maintenance of animal (particularly spiders, snakes, and worms) or blood-injection- injury phobias. Onset can occur indirectly by observing oth- ers reacting fearfully. Some stimuli are more likely to induce phobias than others (e.g., animals vs. electrical outlets) through evolutionary threat relevance. Phobia onset can be precipitated by relationship problems, relo- cation, employment loss, or economic difficulties. In addition, anxiety, mood, or substance use disorders can co-occur with or predate phobia onset. Substance use disorder can maintain phobic symptoms. Phobia symptoms in adolescence predict adult symptoms but are not a risk factor for developing other anxiety, mood, or substance use disorders.
ETIOLOGY AND PATHOPHYSIOLOGY
ANXIETY DISORDERS IN GENERAL Anxiety disorders are characterized by diverse neuroendocrine, neurotransmitter, and neuroanatomical disruptions, the result of interactions between multiple genetic, environmental, and social factors. Although each disorder may have unique features, this group shares some underlying pathophysiology. Pathologic Alterations in Brain Structure and Function Fear and anxiety are thought to involve two major brain cir- cuits: the limbic system and the prefrontal cortex. In the limbic system, which consists of the amygdala, hippocampus, central nucleus of the amygdala, insular cortex, and cingulate cortex, emotion-processing brain structures generate primitive innate responses to simple, overtly threatening stimuli. Functions of limbic structures include processing emotionally important external stimuli and initiating behavioral responses; mediating expressions of fear, aggression, and defensive behavior; and forming and retrieving emotional and fear-related memories [66; 67]. The prefrontal cortex, comprised of the orbitofrontal cortex and the prefrontal, ventromedial, and dorsomedial prefrontal cortex, dampens emotional responses to anxiety- inducing stimuli. The prefrontal cortex functions to regulate impulses, emotions, and behavior via inhibitory “top-down” control of emotional-processing structures; this works to con- trol impulses and regulate mood [66; 67].
Adult Separation Anxiety Disorder Epidemiology
The lifetime prevalence of adult SEPAD is 6.6% in the general population, 12% to 40% in psychiatric clinic settings, and more than 75% among those seeking treatment at anxiety disorder clinics [61]. In adults with lifetime SEPAD, 22.5% have childhood age of onset that persisted into adulthood, while 77.5% had adult onset. Girls/women show higher overall prevalence than boys/men and substantially higher rates of childhood-onset SEPAD persisting into adulthood [62]. SEPAD and panic disorder are highly comorbid in clini- cal settings. Among adult patients with panic disorder, 53.2%
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