It is three in the afternoon, and you are getting ready to rap the best bars ever written and prove yourself to be better than your opponents. Though you know you have adequately prepared, your palms are sweaty, your knees grow weak, and your arms become heavy. You are experiencing nervousness. While this is a normal reaction to a stressful situation, for three percent of Americans, even in seemingly non-stressful environments, the nervous feelings turn into panic attacks (Locke 2015).
Panic disorder (PD) is characterized by episodic, unexpected panic attacks that occur without a clear trigger and are defined by the rapid onset of intense fear (typically peaking within 10 minutes) (Locke 2015). To be diagnosed with PD, one has to have at least four of the symptoms in the DSM-5 diagnostic criteria (see figure 1), followed by persistent concern over additional panic attacks and maladaptive change in behavior related to the panic attacks ( e.g., avoiding unfamiliar places for fear it might trigger a panic attack) (Locke 2015).
While the cause of PD has yet to be identified, symptoms are thought to be partly the result of disruption in the activity in the “emotional centers” of the brain (Martin 2009). In a study by Lee (2006), using single-photon emission computed tomography (SPECT), they investigated regional cerebral blood flow (rCBF) in twenty-nine participants with panic disorder and compared it to twenty-five healthy controls. In addition to performing a SPECT, researchers gave the participants a panic disorder severity scale (PDSS), a rating scale that measures the severity of a person’s panic attacks and panic disorder symptoms. They found that participants with PD have decreased rCBF on the right superior temporal lobe. They also found an inverse relationship between the blood flow of the right superior temporal lobe and the panic disorder severity, with increased severity correlating to decreased rCBF on the right superior temporal lobe.
This study, plus other studies showing structural abnormalities of temporal lobes in patients with panic disorder (Fontaine 1990), supports the idea that disruption in the temporal lobes causes or at least correlates with the symptoms of PD.
Treatments for PD usually fall within two categories: medication and therapy. Some of the most common medications taken as a first line of defense for PD are selective serotonin reuptake inhibitors (SSRIs) and tricyclic antidepressants (TCAs)(Locke 2015). Besides medication, people with PD often undergo cognitive behavioral theory, which applies many techniques like relaxation, exposure therapy, breathing, cognitive restructuring, or education (Locke 2015).
While medication or psychotherapy is usually an initial treatment option for PD, some studies suggest that combining medication and psychotherapy may be more effective for patients with severe symptoms. A study by Kolek (2019) investigated the effectiveness of combining antidepressants with cognitive behavioral therapy in patients with treatment-resistant panic disorder. In this study, the researchers gave one hundred five participants who were pharmacoresistant (patients who were unsuccessfully treated by antidepressants for a minimum of three months) their usual antidepressant dosage range combined with cognitive-behavioral therapy.
The researcher also gave the participants several rating scales before and after the 6-week experiment. The four rating scale that are of importance were a Clinical Global Impression (CGI), which is an assessment of the severity of psychopathology, Beck Anxiety Inventory (BAI), which is an assessment of anxiety symptoms in the last week, Beck Depression Inventory (BDI), which is an assessment of depressive symptoms, and Panic Disorder Severity Scale (PDSS), which is an assessment of the severity of the panic disorder. Researchers found that adding cognitive behavioral therapy decreases the score for all 4 rating scales, supporting the use of both therapy and antidepressant in patients with treatment-resistant panic disorder.
While researching this topic, I found it interesting that a combination of therapy and antidepressants is not the first line of defense after PD, but it is usually either medication or therapy. I wonder why doctors do not offer both options off-front. Since both therapy and medication are equally effective at combating PD (Locke 2015), I wonder if patients’ (and cultural) attitude toward therapy and medication is a deciding factor on whether a psychiatrist advises their patients to go to therapy or take medication for their PD.
Additionally, education as a form of therapy for PD really surprised me, but patient education itself can help reduce anxiety in people with PD (Shearer 2007). This makes sense as some of the symptoms of PD are fear of losing control and fear of dying (many often perceive their panic attack to be a heart attack) (Locke 2015). Knowing what is happening to you and the pathways you can take to possibly get better may reduce these symptoms and contribute to the decrease in anxiety seen in patients educated on PD.
Locke, A. B., Kirst , N., & Shultz, C. (2015). Diagnosis and Management of Generalized Anxiety Disorder and Panic Disorder in Adults. American Family Physician , 1(19), 617–624. Retrieved April 21, 2020, from American Family Physician.
Martin, E. I., Ressler, K. J., Binder, E., & Nemeroff, C. B. (2009). The Neurobiology of Anxiety Disorders: Brain Imaging, genetics, and psychoneuroendocrinology. Psychiatric Clinics of North America, 32(3), 549–575. https://doi.org/10.1016/j.psc.2009.05.004
Engel, K., Bandelow, B., Gruber, O., & Wedekind, D. (2008). Neuroimaging in anxiety disorders. Journal of Neural Transmission, 116(6), 703–716. https://doi.org/10.1007/s00702-008-0077-9
Lee, Y. S., Hwang, J., Kim, S. J., Sung, Y. H., Kim, J., Sim, M. E., Bae, S. C., Kim, M. J., & Lyoo, I. K. (2006). Decreased blood flow of temporal regions of the brain in subjects with panic disorder. Journal of Psychiatric Research, 40(6), 528–534. https://doi.org/10.1016/j.jpsychires.2005.08.012
Fontaine, R., Breton, G., Déry, R., Fontaine, S., & Elie, R. (1990). Temporal Lobe Abnormalities in panic disorder: An MRI study. Biological Psychiatry, 27(3), 304–310. https://doi.org/10.1016/0006-3223(90)90004-l
Shearer SL. Recent advances in the understanding and treatment of anxiety disorders. Prim Care. 2007;34(3):475–504, 5-4.
Kolek, A. Prasko, J. Ociskova, M. Holubova, M. Vanek, J. Grambal, A. (2019). Slepecky M. Severity of panic disorder, adverse events in childhood, dissociation, self-stigma and comorbid personality disorders Part 2: Therapeutic effectiveness of a combined cognitive behavioral therapy and pharmacotherapy in treatment-resistant in patients. Neuro Endocrinol Lett, 40(6):271-283. PMID: 32200586.