Panic disorder
Panic disorder is a mental and behavioral disorder,[5] specifically an anxiety disorder characterized by reoccurring unexpected panic attacks.[1] Panic attacks are sudden periods of intense fear that may include palpitations, sweating, shaking, shortness of breath, numbness, or a feeling that something terrible is going to happen.[1][2] The maximum degree of symptoms occurs within minutes.[2] There may be ongoing worries about having further attacks and avoidance of places where attacks have occurred in the past.[1]
Panic disorder
Sudden periods of intense fear, palpitations, sweating, shaking, shortness of breath, numbness[1][2]
Sudden and recurrent[1]
Unknown[3]
Family history, smoking, psychological stress, history of child abuse[2]
Heart disease, hyperthyroidism, drug use[2][3]
2.5% of people at some point[4]
The cause of panic disorder is unknown.[3] Panic disorder often runs in families.[3] Risk factors include smoking, psychological stress, and a history of child abuse.[2] Diagnosis involves ruling out other potential causes of anxiety including other mental disorders, medical conditions such as heart disease or hyperthyroidism, and drug use.[2][3] Screening for the condition may be done using a questionnaire.[6]
Panic disorder is usually treated with counselling and medications.[3] The type of counselling used is typically cognitive behavioral therapy (CBT) which is effective in more than half of people.[3][4] Medications used include antidepressants, benzodiazepines, and beta blockers.[1][3] Following stopping treatment up to 30% of people have a recurrence.[4]
Panic disorder affects about 2.5% of people at some point in their life.[4] It usually begins during adolescence or early adulthood, but may affect people of any age.[3] It is less common in children and elderly people.[2] Women are more likely than men to develop panic disorder.[3]
Causes[edit]
Psychological models[edit]
While there is not just one explanation for the cause of panic disorder, there are certain perspectives researchers use to explain the disorder. The first one is the biological perspective. Past research concluded that there is irregular norepinephrine activity in people who have panic attacks.[16] Current research also supports this perspective as it has been found that those with panic disorder also have a brain circuit that performs improperly. This circuit consists of the amygdala, central gray matter, ventromedial nucleus of the hypothalamus, and the locus ceruleus.[17]
There is also a cognitive perspective. Theorists believe that people with panic disorder may experience panic reactions because they mistake their bodily sensations for life-threatening situations.[18] These bodily sensations cause some people to feel as though are out of control which may lead to feelings of panic. This misconception of bodily sensations is referred to as anxiety sensitivity, and studies suggest that people who score higher on anxiety sensitivity surveys are five times more likely to be diagnosed with panic disorder.[19]
Panic disorder has been found to run in families, which suggests that inheritance plays a strong role in determining who will get it.[20]
Psychological factors, stressful life events, life transitions, and environment as well as often thinking in a way that exaggerates relatively normal bodily reactions are also believed to play a role in the onset of panic disorder. Often the first attacks are triggered by physical illnesses, major stress, or certain medications. People who tend to take on excessive responsibilities may develop a tendency to have panic attacks. Individuals with post-traumatic stress disorder (PTSD) also show a much higher rate of panic disorder than the general population.[21]
Prepulse inhibition has been found to be reduced in patients with panic disorder.[22]
Substance use[edit]
Substance use disorders are often correlated with panic attacks. In a study, 39% of people with panic disorder had recreationally used substances. Of those who used alcohol, 63% reported that the alcohol use began prior to the onset of panic, and 59% of those using illicit substances reported that substance use began first. The study that was conducted documented the panic-substance use disorder relationship. Substance use disorder began prior to the onset of panic and substances were used to self-medicate for panic attacks by only a few subjects.[23]
In another study, 100 methamphetamine-dependent individuals were analyzed for co-morbid psychiatric disorders; of the 100 individuals, 36% were categorized as having co-morbid psychiatric disorders. Mood and Psychotic disorders were more prevalent than anxiety disorders, which accounted for 7% of the 100 sampled individuals.[24]
Mechanism[edit]
The neuroanatomy of panic disorder largely overlaps with that of most anxiety disorders. Neuropsychological, neurosurgical, and neuroimaging studies implicate the insula, amygdala, hippocampus, anterior cingulate cortex (ACC), lateral prefrontal cortex, and periaqueductal grey. During acute panic attacks, viewing emotionally charged words, and rest, most studies find elevated blood flow or metabolism. However, the observation of amygdala hyperactivity is not entirely consistent, especially in studies that evoke panic attacks chemically. Hippocampus hyperactivity has been observed during rest and viewing emotionally charged pictures, which has been hypothesized to be related to memory retrieval bias towards anxious memories. Insula hyperactivity during the onset of and over the course of acute panic episodes is thought to be related to abnormal introceptive processes; the perception that bodily sensations are "wrong" is a transdiagnostic finding (i.e. found across multiple anxiety disorders), and may be related to insula dysfunction. Rodent and human studies heavily implicate the periaqueductal grey in generating fear responses, and abnormalities related to the structure and metabolism in the PAG have been reported in panic disorder. The frontal cortex is implicated in panic disorder by multiple lines of evidence. Damage to the dorsal ACC has been reported to lead to panic disorder. Elevated ventral ACC and dorsolateral prefrontal cortex during symptom provocation and viewing emotional stimuli have also been reported, although findings are not consistent.[59]
Researchers studying some individuals with panic disorder propose they may have a chemical imbalance within the limbic system and one of its regulatory chemicals GABA-A. The reduced production of GABA-A sends false information to the amygdala which regulates the body's "fight or flight" response mechanism and, in return, produces the physiological symptoms that lead to the disorder. Clonazepam, an anticonvulsant benzodiazepine with a long half-life, has been successful in keeping the condition under control.[60]
Recently, researchers have begun to identify mediators and moderators of aspects of panic disorder. One such mediator is the partial pressure of carbon dioxide, which mediates the relationship between panic disorder patients receiving breathing training and anxiety sensitivity; thus, breathing training affects the partial pressure of carbon dioxide in a patient's arterial blood, which in turn lowers anxiety sensitivity.[61] Another mediator is hypochondriacal concerns, which mediate the relationship between anxiety sensitivity and panic symptomatology; thus, anxiety sensitivity affects hypochondriacal concerns which, in turn, affect panic symptomatology.[62]
Perceived threat control has been identified as a moderator within panic disorder, moderating the relationship between anxiety sensitivity and agoraphobia; thus, the level of perceived threat control dictates the degree to which anxiety sensitivity results in agoraphobia.[63] Another recently identified moderator of panic disorder is genetic variations in the gene coding for galanin; these genetic variations moderate the relationship between females with panic disorder and the level of severity of panic disorder symptomatology.[64]
The DSM-IV-TR diagnostic criteria for panic disorder require unexpected, recurrent panic attacks, followed in at least one instance by at least a month of a significant and related behavior change, a persistent concern of more attacks, or a worry about the attack's consequences. There are two types, one with and one without agoraphobia. Diagnosis is excluded by attacks due to a drug or medical condition, or by panic attacks that are better accounted for by other mental disorders.[65]
The ICD-10 diagnostic criteria:
The essential feature is recurrent attacks of severe anxiety (panic), which are not restricted to any particular situation or set of circumstances and are therefore unpredictable.
The dominant symptoms include:
Panic disorder should not be given as the main diagnosis if the person has a depressive disorder at the time the attacks start; in these circumstances, the panic attacks are probably secondary to depression.[66]
The Panic Disorder Severity Scale (PDSS) is a questionnaire for measuring the severity of panic disorder.[67]
Children[edit]
A retrospective study has shown that 40% of adult panic disorder patients reported that their disorder began before the age of 20.[109] In an article examining the phenomenon of panic disorder in youth, Diler et al. (2004)[110] found that only a few past studies have examined the occurrence of juvenile panic disorder. They report that these studies have found that the symptoms of juvenile panic disorder almost replicate those found in adults (e.g. heart palpitations, sweating, trembling, hot flashes, nausea, abdominal distress, and chills).[111][112][113][114][115] The anxiety disorders co-exist with staggeringly high numbers of other mental disorders in adults.[116] The same comorbid disorders that are seen in adults are also reported in children with juvenile panic disorder. Last and Strauss (1989)[117] examined a sample of 17 adolescents with panic disorder and found high rates of comorbid anxiety disorders, major depressive disorder, and conduct disorders. Eassau et al. (1999)[113] also found a high number of comorbid disorders in a community-based sample of adolescents with panic attacks or juvenile panic disorder. Within the sample, adolescents were found to have the following comorbid disorders: major depressive disorder (80%), dysthymic disorder (40%), generalized anxiety disorder (40%), somatoform disorders (40%), substance abuse (40%), and specific phobia (20%). Consistent with this previous work, Diler et al. (2004) found similar results in their study in which 42 youths with juvenile panic disorder were examined. Compared to non-panic anxiety disordered youths, children with panic disorder had higher rates of comorbid major depressive disorder and bipolar disorder.
Children differ from adolescents and adults in their interpretation and ability to express their experience. Like adults, children experience physical symptoms including accelerated heart rate, sweating, trembling or shaking, shortness of breath, nausea or abdominal pain, dizziness or light-headedness. In addition, children also experience cognitive symptoms like fear of dying, feelings of being detached from oneself and feelings of losing control or going crazy. Children are often unable to articulate these higher-order manifestations of fear; they simply feel that something is wrong and that they are very afraid. Children can only describe physical symptoms. They have not yet developed the ability to put these symptoms together and label them as fear. Parents often feel helpless when they watch their child suffer. They can help children give a name to their experience, and empower them to overcome the fear they are experiencing[118]
The role of the parent in treatment and intervention for children diagnosed with panic disorder is discussed by McKay & Starch (2011). They point out that there are several levels at which parental involvement should be considered. The first involves the initial assessment. Parents, as well as the child, should be screened for attitudes and treatment goals, as well as for levels of anxiety or conflict in the home. The second involves the treatment process in which the therapist should meet with the family as a unit as frequently as possible. Ideally, all family members should be aware and trained in the process of cognitive behavior therapy (CBT) in order to encourage the child to rationalize and face fears rather than employ avoidant safety behaviors. McKay & Storch (2011) suggest training/modeling of therapeutic techniques and in-session involvement of the parents in the treatment of children to enhance treatment efficacy.[119]
Despite the evidence pointing to the existence of early-onset panic disorder, the DSM-IV-TR currently only recognizes six anxiety disorders in children: separation anxiety disorder, generalized anxiety disorder, specific phobia, obsessive-compulsive disorder, social anxiety disorder (a.k.a. social phobia), and post-traumatic stress disorder. Panic disorder is notably excluded from this list.