Panic disorder

Panic disorder

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Panic disorders and panic attacks are frequent medical issues in psychiatric clinics. Panic disorder is a type of anxiety disorder described by repetitive and spontaneous panic attacks. The frequency can vary from several attacks daily to very few in a year. A person with panic disorder experiences a sudden surge of extreme fear that peaks within ten minutes. According to the DSM-5, four or more of the thirteen known symptoms must be present for a definitive diagnosis of panic disorder to be made. The symptoms include palpitations, tachycardia, sweating, dyspnea, a feeling of choking, chest pain, nausea, vomiting, light-headedness, paresthesias, depersonalization, and the fright of dying or going out of control (Cackovic, Nazir & Marwaha, 2020). The worst scenario is when panic attacks occur without the presence of precipitating conditions. Such patients are the toughest to manage. Panic attacks occur alongside anxiety, mood, psychotic, or substance abuse disorders. Panic disorder affects one’s quality of life; they are more predisposed to depression and alcoholism.

The lifetime prevalence of the condition is high, ranking fourth to social anxiety disorder, PTSD, and generalized anxiety disorder. In addition, these persons are more susceptible to cardiovascular, GIT, and respiratory diseases than the general population. There is a 2-6% lifetime prevalence risk in American adults. The annual prevalence in adults is 2.7%. 44.8% of the cases are severe. These patients often go into depression if proper management is not followed. The persons share comorbidities with COPD, IBS, fatigue, migraines, and restless leg syndrome. Pregnant women with panic disorders give birth to underweight or preterm babies (Meuret, Kroll & Ritz, 2017). Clinicians need to stabilize persons with both panic disorders and comorbid coronary arterial disease since these persons are predisposed to myocardial ischemia during the episodes. Hence, special monitoring is necessary for this fraction of the population. Asthmatic patients have a 4.5-time risk of getting panic disorders. On the other hand, persons with panic disorders have a 6-time risk of developing asthma. Generally, European Americans are more susceptible to panic disorders than African-Americans or Latinos. The black communities regularly present with somatic symptoms. Men are 2-3 times less likely to get panic disorders than women. Among women, those who have never conceived are more vulnerable than those who have become pregnant. Panic attacks occur at any age. The average age is 24 years, however, it can occur to persons between the ages of 18-45 years. Those with a late-onset age, have a better outcome than those with early-onset (Bandelow & Michaelis, 2015). Late-onset patients have better-coping characters and are less likely to get admitted to psychiatric facilities. They are also less prone to substance abuse.

There are several explanations elucidated on the causes of panic disorders. The first one uses a psychological model as its baseline. The biological perspective links the role of norepinephrine to the manifestation of the disease. The brain circuit of these individuals displays abnormalities in function. The circuit connects functionality of the amygdala, the locus ceruleus, central gray matter, and the hypothalamus. The model proposes that these persons have dysfunctional cognitive abilities that mistake normal body senses for dangerous states. It is a condition similar to hypersensitivity reactions where the body overreacts to friendly or harmless substances. As a result, the persons feel as though they are losing control, which leads to overt behavior.

Secondly, scientists have tried to relate substance abuse to the onset of panic attacks. The results are overwhelming but not conclusive. A single study showed that 39% of persons with panic disorders had used these substances. 63% of those who drink alcohol reported that they began taking it before the onset of panic disorders; a further 59% of those who took other substances also reported that their abuse began before panic attacks (Bandelow & Michaelis, 2015). Hence, there may be a link between the use of these substances of abuse to panic disorders. Tobacco smoking is one of the most commonly abused substances. The link to panic attacks is strong. However, it is still not clear how smoking causes the development of panic episodes. Some studies hypothesize that the onset may be due to changes in respiratory function. Nicotine withdrawal leads to anxiety and panic disorders. Stimulants such as caffeine may also precipitate the aforementioned disorders in vulnerable people (Cackovic, Nazir & Marwaha, 2020). Other stimulants include pseudoephedrine, ephedrine, oxymetazoline, and phenylephrine.

Panic disorders share similar neuroanatomy with other anxiety disorders. Psychological studies, neurosurgery, and neuro-images associate various regions of the brain; amygdala, hippocampus, lateral prefrontal cortex, and insula. Observational studies on the amygdala report increased blood flow to these regions when emotionally charged words are spoken. The hippocampus is also a culprit because parallel studies show similar results when emotionally charged pictures are presented to the person. There are several loopholes in these results. Hence, it is not easy to make conclusions. Some of the studies are done on rodents, while others are done on human beings. Human beings’ brain studies must meet ethical criteria. The researchers have a lot on their hands. They must come up with practical and suitable models to facilitate thorough studies. Other studies propose an association between the limbic system to the GABA-A system. GABA-A exerts regulatory function on the limbic system. Hence, a low level of the GABA neurotransmitter causes inappropriate functioning of the amygdala which is involved in the body’s fight or flight mechanism (Cackovic, Nazir & Marwaha, 2020). Clinically, this is translated as the feeling of losing control, fear, or being in life-threatening circumstances. Some studies are focused on the role of chemical mediators in panic disorders. For example, partial pressures of carbon dioxide in the body regulate the rate and depth of breathing in the body. When the partial pressures of carbon dioxide rise, an individual hyperventilates to get rid of the excess CO2 in the body. The converse is true at low partial pressures of CO2 (Cackovic, Nazir & Marwaha, 2020). There may be a link between the partial pressures of CO2 and the onset of anxiety. Persons with anxiety disorders undergo breathing training to relieve anxiety symptoms. Hence, the partial pressures of CO2 may be regulatory to brain activities.

Genetic factors are important in understanding the prevalence of panic disorders. First-degree relatives of persons with the condition have a lifetime prevalence risk of about 43% (Cackovic, Nazir & Marwaha, 2020). The genetic basis of the condition is clear but the genes responsible are yet to be elucidated. The current understanding suggests the role of multiple genes in the development of panic disorders. Environmental factors coalesce with these genes to cause brain abnormalities responsible for the clinical symptoms. MAOIs are useful medications in the management process. Hence, it is logical that monoamine oxidase genes may play a role in the disease. The COMT genes are prone to polymorphism. Therefore, persons who inherit homozygous genes in which valine replaces methionine at position 158 are more vulnerable to panic disorders than those who lack these genes or those who inherit heterozygous genes (Carter, 2019).

There are no precise lab or radiographic tests available to diagnose this condition. Diagnosis relies on the DSM-V criteria. A diagnosis is made when there are regular abrupt panic episodes, which are followed by one or more months of obstinate concern over having another attack, and also an alteration in behavior to avoid the previous precipitating conditions. Panic episodes due to medications, substance abuse, hyperthyroidism, or vestibular dysfunction must be eliminated from this list for a proper diagnosis to be made. The aforementioned symptoms are necessary and are included in the clinical workup. The Panic Disorder Severity Scale is a useful questionnaire for determining the severity of these episodes (Substance et al., 2016).

There is no cure for panic disorder. The main treatment approach utilizes both psychological and pharmacological methods. Cognitive Behavioral Therapy and positive self-talk are the treatment of choice for panic disorders. CBT emphasizes the need to embrace the known precipitant of these attacks. The rationale is based on the ability of the brain to reduce its sensitivity to these triggers. Hence, once the brain becomes used to these triggers there is a reduced probability that the person will have issues. The journey commences with calming breathing training, followed by observing alterations in physical senses. Hyperventilation must be kept at a minimum or eradicated. Psychotherapy can be used alone or combined with benzodiazepines. Various techniques are employed such as straw breathing, body tensing, intentional hyperventilation, breath-holding, running around to increase the heart rate, or spinning in a chair. Therapists must evoke anxiety emotions to get to the root cause. 85% of persons on CBT get a good prognosis (Milrod et al., 2016). Persons with comorbid depression, alcohol abuse, or personality disorders have poor outcomes. Family support groups can help improve prognosis. Selective serotonin reuptake inhibitors (SSRIs) are the drugs of choice for panic disorders. Benzodiazepines use is associated with tolerance, dependence, and abuse. Their use is still controversial. MAOIs, TCAs, and Norepinephrine Reuptake Inhibitors are useful alternatives (Hindman & Beck, 2015). Suicidal patients must be monitored when on these drugs since some of them intensify suicidal thoughts.

Panic disorder rarely occurs independently. More often than not, most persons experience a relapse in their symptoms. Compliance with treatment approaches is a critical issue to enhance remission. However, relapses are frequent. Approximately, 60% of the patients attain remissions within six months. Patients with excellent premorbid conditions and a short period of symptoms tend to better prognosis. A small proportion of 10-20% continues to manifest substantial symptoms. The risk of CAD in these patients doubles (Cackovic, Nazir & Marwaha, 2020).

Patient education is an aftermath of evidence-based medical practice. The patient is at the center of all treatment approaches and should be treated as such. Hence, it is essential to inform the patient about the diagnosis and treatment options (Antony & Barlow, 2020). The clinician should tell the patient about the potential adverse drug reactions. A comprehensive care plan should provide details of how to identify trigger stimuli. The therapist should sit down with the patient and his or her family and provide counsel about the disease. He or she should tell them that the disease is not life-threatening nor communicable. To the family member, the therapist should encourage them to provide psychosocial support since it improves the therapeutic outcome. Encourage family members to ensure therapeutic compliance and a healthy lifestyle. Alcohol consumption should be avoided. Probably, the simplistic approach is what is needed to improve prognosis. The mentioned counsel is simple to follow and ignore at the same time. Hence, the clinician should emphasize this at each clinical visit.

References

Antony, M. M., & Barlow, D. H. (Eds.). (2020). Handbook of assessment and treatment planning for psychological disorders. Guilford Publications.

Bandelow, B., & Michaelis, S. (2015). Epidemiology of anxiety disorders in the 21st century. Dialogues in clinical neuroscience, 17(3), 327.

Cackovic, C., Nazir, S., & Marwaha, R. (2020). Panic disorder (attack). StatPearls [Internet].

Carter, R. (2019). The human brain book: An illustrated guide to its structure, function, and disorders. Penguin.

Hindman, R., & Beck, J. S. (2015). A Clinical Handbook of Psychological Disorders: A Step-by-Step Treatment Manual.

Meuret, A. E., Kroll, J., & Ritz, T. (2017). Panic disorder comorbidity with medical conditions and treatment implications. Annual review of clinical psychology, 13, 209-240.

Milrod, B., Chambless, D. L., Gallop, R., Busch, F. N., Schwalberg, M., McCarthy, K. S., … & Barber, J. P. (2016). Psychotherapies for panic disorder: A tale of two sites. The Journal of Clinical Psychiatry, 77(7), 927-935.

Substance, A., Mental, H. S. A. U., & Office of the Surgeon General (US. (2016). Facing addiction in America: The Surgeon General’s report on alcohol, drugs, and health.