Essay: Panic disorders

Panic disorder is one of the most prevalent psychiatric diseases in the mental health community affecting approximately 4% of the population in their lifetime (Fava & Morton, 2009). It is characterized by recurrent panic attacks that manifest itself suddenly with physiological symptoms of fear and danger (Clark, 1986 as cited by Fava & Morton, 2009). Although patients are not actually in any imminent danger, psychologically they feel as if they were and thus their bodies respond accordingly with symptoms such as tachycardia, sweating and hyperventilation (Clark, 1986 as cited by Fava & Morton 2009). Panic Disorder therefore leads to a severe disruption in patients’ lives because, depending on severity, they are not able to function at a normal level due to impending attacks.
Studies have long tried to find a determinate cause of panic disorder; however, there has still yet to be one found that can explain why some people develop panic disorder while others do not. Many studies have generalized panic disorder as a more severe form of anxiety disorder and thus when looking for a cause, the study focuses on what causes that one behavior (Fava & Morton, 2009). There have been studies that focus on the social triggers of panic disorder and past life events that led up to the diagnosis of panic disorder. However, although a specific event may cause one person to have panic attacks someone with the same experiences may not. Therefore, there seems to be some another component that causes one person to develop the disorder while others do not. Biological or genetic variations seem to be the most logical reason for differences between those who develop the disorder and those who do not since social or cognitive causation cannot fully explain the development of the disorder.
Countless studies have suggested that biological abnormalities in the fear center of the brain may be what cause the development of the disorder in patients (Fava & Morton, 2009). Initially, researchers located the areas of the brain associated with fear by testing symptoms of anxiety in animals. Through extensive animal research, done on mostly rodents, researchers have been able to locate specific areas of the brain for causes and therefore treatment of panic disorder (Richter et al., 2012). The fear network of the brain in animals that causes anxiety has also been revealed to cause anxiety in the brains of human beings as well (Gratacos et al., 2007).
The fear network of the brain begins with the amygdala. In general, the amygdala processes emotions and translates the emotions into reactions by triggering other parts of the brain through neurotransmitters (Gratacos et al., 2007). The amygdala works in conjunction with areas of the brain such as the brainstem and prefrontal cortex which is activated by a series of chemicals in the brain which in turn leads to the physiological symptoms of the disorder such as rapid breathing and sweating. Then, the cognitive centers of the brain are also activated by these same chemicals to create an association between what triggered the attack and anxiety. This in turn creates a vicious cycle where many panic disorder patients develop intense phobias to what they think triggers their panic attacks (Gratacos et al., 2007). Gorman, Kent, Sullivan, & Coplan (2000) proposed a mechanism to this phenomenon and called it the Neuroanatomical Hypothesis of Panic Disorder. The hypothesis essentially states that the fear network of the brain in patients with panic disorder is more easily activated than in people without the disorder and the things that activate the symptoms in the amygdala are stored as memories in the hippocampus. The phobias are the result of the memories in the hippocampus being triggered and then those activating the amygdala which activates the rest of the parts of the fear center of the brain (Gorman, Kent, Sullivan & Coplan, 2000). This in turn, ends up leading to more anxiety in the patient because they are constantly worried that they will encounter the trigger again and have another panic attack.
In order to test for the active areas in the brain during panic attacks in patients, most researchers have resorted to brain imaging to map out the brain (Fava & Morton, 2009). However, it is very difficult to capture the brain in action during panic attacks and thus most researchers use brain imaging such as fMRIs and PET to locate any abnormalities that are consistent in patients with panic disorder (Richter et al., 2012). During the course of their experiment Kim et al., (2007) found that there are a few slight differences in the brains of patients with panic disorder and those without the disorder; however, the sample size was very small during the experiment and thus the findings are still inconclusive. For the findings of the experiment to be significant, a larger number of patients with panic disorder would need to have their brains scanned (Kim et al., 2007). If researchers can find a way to run brain imaging while the patient is having a panic attack then eventually, it may reveal a physical abnormality in the brain of patients with panic disorder. However, researchers have managed to use other methods to test for biological differences and map out the areas of the brain being activated during panic attacks in patients besides brain imaging.
In combination with neuroimaging, researchers do still run basic behavioral experiments on patients with panic disorder to test for neurological abnormalities in the patients. During Richter et al., (2012)’s experiment patients were held in a dark room for a specified amount of time and then not only was their normal physiological measurements recorded, such as heart rate, but also each person’s behavior was observed. The behaviors were then categorized into three groups and correlated with the intensity of physiological change in each patient. The results of the experiment support the Neuroanatomical Hypothesis for Panic Disorder in that during subsequent tests the memory of the thought of danger in the darkness triggered panic attacks in a few of the patients during the experiment (Richter et al., 2012) . These panic attacks were successfully recorded by the researchers in the form of extreme increase of patients’ heart rate and also a significant increase of perspiration on the patient; also a panic button was pressed by the patient during the experiment to signify their acknowledgement that they were having a panic attack at the specific moment during the experiment (Richter et al., 2012). Also, although the experiment focuses almost exclusively on perspiration and heart rate, with these changes in physiological responses in the patients it can be assumed that hypoxia was also noted in the patients during the panic attacks since hyperventilation is a notable sign of a patient having a panic attack.
Throughout the early years of the study of panic disorder, most researchers focused on hyperventilation as a cause of panic attacks in patients with panic disorder; however, in recent studies although hyperventilation does cause a change in brain chemistry it is more likely symptom rather than a cause of the disorder (Maddock, Buonocore, Copeland, & Richards, 2009). Hyperventilation has long been associated with panic attacks and early studies concluded that the low oxygen levels and increase in carbon dioxide in the body caused a low pH level in the brain which was what caused the panic attacks in patients (Sikter, Frecska, Braun, Gonda, & Riner, 2007). However, Maddock, Buonocore, Copeland, & Richards (2009) showed in their research that other chemicals can cause the same reactions in the brain as hyperventilation and could be a cause of panic attacks in patients as well. During the course of their experiment, the researchers tested sodium lactate which produced the same effects as hyperventilation and also seemed to be in higher concentration in panic disorder patients than healthy controls (Maddock, Buonocore, Copeland, & Richards, 2009). The results of this experiment coincide with the theory that chemicals in the brain produce the symptoms of panic attacks.
One such chemical that has become recurrent in recent studies of panic disorder is the study of the effect of the neuropeptide cholecystokinin or CCK on the brain. CCK was first known for being a hormone that worked exclusively in the digestive system, however it was discovered later on that CCK was also active in the brain and specifically active in the areas of the brain that trigger fear and anxiety (Zwanger, Domsche, & Bradwejn, 2012). One experiment found that variants of the neuropeptide correlated strongly with the development of panic disorder in patients and also bipolar disorder, which is another psychiatric disorder that is often associated with panic disorder besides agoraphobia (Fitches, Markie, & Wilson, 2012). However, the experiment was unable to directly link CCK with panic disorder thus leading to inconclusive results as to whether CCK itself can directly cause panic disorder or if it was another symptom (Fitches, Markie, & Wilson, 2012). But, animal testing in rodents has established that CCK does at least cause anxiety in the brain and then further testing revealed that the administration of CCK can cause anxiety in human patients (Gratacos et al., 2007). In their study of CCK on the brain, Zwanger, Domsche, & Bradwejn (2012) ultimately proposed that it was possible abnormality in the amount of CCK being released in the amygdala could cause panic disorder in patients. The excess CCK in the brain triggers the amygdala to activate thus causing a chain reaction of fear and anxiety in patients. They also propose that genetics may be what causes this anomaly in the fear centers of the brain in patients that develop panic disorder (Zwanger, Domsche, & Bradwejn, 2012).
With the increase of genetic and DNA study, researchers have combined the use of neuroimaging with genetic study to test if there is a genetic component tied to any abnormalities that they may find in the brain of patients with panic disorder (Kim et al., 2007). Several studies have begun to use blood testing to pinpoint genotypes that may be connected with the disorder and often use the Hardy-Weinberg Equilibrium in conjunction with their tests (Otawa et al., 2011). Gratacos et al., (2007) proposed that two types of genetic variations could lead to the development of panic disorder in patients. The first type would coincide with the theory of CCK as mentioned earlier in that a genetic variation can cause in influx of neurotransmitters in the brain thus causing an over activation in the fear center and therefore leading to symptoms of panic disorder. The second type would mean a direct genetic abnormality in the fear center itself, such as damage to the amygdala which led to an increased sensitivity of that part of the brain. This would mean that although the patient is releasing the same amount of neurotransmitters the amygdala would react more strongly with it thus triggering a panic attack and leading to the development of panic disorder (Gratacos et al., 2007). One particular study correlated with the second type of genetic anomaly, in that it tested two different genotypes of patients with panic disorder and found that one particular genotype was associated with a difference in the myelination of the white matter inside of the brain (Kim et al., 2012). However, a few studies have showed that this type of genetic anomaly that causes panic disorder may be gender associated.
Recent studies have begun correlating genetic variations in panic disorder with gender. Although, it is inconclusive as to whether panic disorder is a genetic disorder at least one study associated a genetic difference between female patients with panic disorder and male patients with panic disorder (Otawa et al., 2011). This may mean that gender makes a difference in how panic disorder is developed; based off of this study it can be hypothesized that etiology of panic disorder can be different based on gender. Then, not only does there appear to be a genetic difference between the genders but also a behavioral difference. During a behavioral experiment of panic disorder, females were more likely to show higher amount of anxiety and fear than their male counterparts (Richter et al., 2012). Also, Hohoff et al., (2007) experiment supports the theory that the development of panic disorder can be different based on gender due to a genetic variant being found mainly in the female population of patients but not the male population. This same experiment also revealed that a particular genotype was very rare in both female and male patients with panic disorder; therefore it is possible that some people have a protective gene against the development of the disorder (Hohoff et al., 2007). However, the entire population of this study was also of only one specific ethnicity, German, and this makes the findings of this study inconclusive because studies have also supported the hypothesis that not only does gender play a role in how genetics play a role in the development of panic disorder but also ethnicity.
Due to ethnic mixture in the United States it can be assumed that most American studies in regards to panic disorder represent the racial diversity of the population; however, the same cannot be said of studies conducted in other countries where almost 100 percent of the population is of one ethnicity. Many studies that have made significant findings in regards to genetic anomalies in patients with panic disorder have also had a sample set comprised entirely of patients of one ethnicity. Kim et al., (2012) made a significant finding in a specific genotype that causes a change in white matter connectivity in the brain of patients however; all of the patients in the study were Korean. The researchers concluded that although this finding was significant the genetic variation was found mostly in an Asian population and not a Caucasian population (Kim et al., 2012). The opposite could be said of Otawa et al., (2011) experiment which did not find a significant difference between the gene they were studying in patients with panic disorders and a healthy control. The experiment was composed of an entirely Japanese population and it is possible that in an all Caucasian or African population, the genetic variant may be of significance. Also, more research needs to be conducted in regards to genetic differences in patients of African and Latin descent to establish whether the same genetic variances can be found in those populations as well or if they also have their own genetic variations that correlate with the development of panic disorder.
There are many implications for neurobiological differences in the brain that causes panic disorder; however it’s not exactly sure where these differences are coming from. There is some evidence that genes play a role in how the brain is functioning and causing the disorder. Genes could be causing an over sensitivity in the fear network of the brain and thus causing the disorder or it could creating an abnormality in the fear center of the brain itself. However, one genetic abnormality has yet to be pinpointed and it appears that more than one genetic anomaly leads to the same outcome. Also, there is evidence that there are gender differences in the disorder in that female patients with panic disorder may get the disorder from a different cause than male patients with panic disorder. This supports the theory that there is more than more neurobiological cause for the disorder and that the abnormalities work in conjunction with each other for the development of the psychiatric disorder in patients. However, more research needs to be done in regards to not only gender differences but also racial differences that could be making a difference in the development of the disorder. Researchers will need to conduct and also repeat more experiments to eventually find a determinate cause of the disorder if there is one determinate cause at all.