Generalized anxiety disorder
-By Timothy Lyons
Generalized anxiety disorder is a disorder that is characterized by anxiety. The type of anxiety that accompanies a diagnosis of generalized anxiety disorder is constant and relentless. The type of anxious thinking that occurs is not confined to any specific environmental situation. It is not attached or directed. Although there is no overarching fixation for the worry it can often involve fears over illness or accidents of the sufferer or their family. The prominent symptoms often include nervousness, trembling, muscle tension, feeling lightheaded, dizzy, sweats or stomach problems (World Health Organization, 2016).
One main feature is that the worry itself is spread out over many different topics or events. It is most likely that the magnitude, timespan and recurrence of the anxiety and worry is not proportional to the chance the event will occur or to its severity. In most cases the sufferer cannot control the intrusive thoughts and has difficulty paying attention to current undertakings. The worries can center on mundane everyday events like chores and appointments but it is often the case that the worry shifts from topic to topic (American Psychiatric Association, 2013).
From a clinical standpoint it is necessary to differentiate this disorder from anxiety that does not impede on one’s life. The thoughts worries and anxiety of the disorder interfere with routine psychological and social operations. These worries are unmanageable and are intrusive to the point of taking precedent over other matters. The focus of the prevalent worries cause distress and are of a long duration. They occur without triggers while the large range of topics about which the person worries make it more likely to receive a diagnosis of generalized anxiety disorder. Physical symptoms such as restlessness and feeling agitated manifest from or accompany the anxiety. In many cases persons with generalized anxiety disorder report problems with work and social life due to constant worrying (American Psychiatric Association, 2013)
Another aspect of generalized anxiety disorder is that in adults, the worry happens along with at least three or more concurrent symptoms. These symptoms include restlessness or feeling keyed up or on edge, being easily fatigued, difficulty concentrating or mind going blank, irritability, muscle tension, and disturbed sleep (American Psychiatric Association, 2013).
In addition, in order for this diagnosis to take place the symptoms of worry must have happened for most of the time for at least six months. They cannot have been as a result of the use of substances or from medications nor can they be as a result of some medical condition such as hypothyroidism. It is also important that the symptoms of this disorder be differentiated from other mental disorders such as anxiety disorder whether induced by medical condition or substance use, obsessive compulsive disorder and even post-traumatic stress disorder (American Psychiatric Association, 2013).
Often generalized anxiety disorder is distinguished by a deficiency in the ability of a person to regulate emotions. In (MacNamara & Proudfit, 2014) it is suggested that the regulation of emotions may be biological with the prefrontal cortex being affected by focus on tasks which then reduces the person’s ability to filter out emotional information. In this case there has been a decrease in wave forms produced while undergoing electro-encephalogram studies which provide evidence that points to possible attention problems in the person affected. The idea is that when there is a depletion of focusing resources in the affected person the attentional control is reduced. This would mean that as the person continues to attempt control of the emotions there is still less resources to control and the emotions then overwhelm the person. Also, the focus is reduced when there is negative stimuli. In this case the negative or disruptive emotions are the cause. The idea that emotion dysregulation is one factor in this puzzle has been held for some time. This study also points to a strong evidence base of comorbidity for depression with the generalized anxiety disorder sufferer which is also another aspect of generalized anxiety disorder that helps to define it. It would appear that this is a type of downward spiral that continues into an anxiety across any number of lifestyle choices for the person experiencing generalized anxiety disorder.
One other important area that assists in definition and description would be rumination. In the study (Ruscio et al., 2015) there is support that rumination contributes to decline in affect, increased depression and anxiety and is associated with psychopathology in life. This supports the earlier study in lessened emotion control. This study shows that rumination may acclimate individuals to be affected by even minor stress which allows for the idea that when faced with events that are not majorly stressful the generalized anxiety disorder is still present. Rumination then is one of the manners in which this disorder can be identified and described.
Defining generalized anxiety disorder would not be complete without some discussion of impairments that are caused by stress and anxiety. Persons diagnosed with generalized anxiety disorder discuss social and occupational impairments. There are often somaticized symptoms such as sweating nausea and bowel problems. Muscle aches, trembling shakiness and twitching are a result of tension in the muscles. Individuals with generalized anxiety disorder report subjective distress which culminates in autonomic issues such as raised heart rate, dizziness and short breath (Ruscio et al., 2015; American Psychiatric Association, 2013). Further, there is evidence that part of the impairment process is informed by thoughts that things are hopeless which pushes the person to excuse themselves to avoid, withdraw or even to complete inaction toward possible stressors. This would then increase tension, stress and muscles aches.
Etiology
So from where does this disorder come? There are often contributing factors such as psychological, neurological, biochemical, genetic, environmental and socio-cultural that are the basis for ideas behind the causes and origins of the disorder.
Psychological
From the psychological standpoint there have been studies such as (Aviram, Westra, Constantino, & Antony, 2016) that discuss client resistance to treatment protocols such as cognitive behavioral therapy with generalized anxiety disorder populations. The resistance is in service of the defense of the clients beliefs. Therapists that can flexibly switch to a motivational interviewing modality have better outcomes. This might point to the fact that rational thinking errors and rumination are active in the generalized anxiety disorder sufferer. Rather than active confrontation of these irrational thoughts the therapist can use the Socratic Method to have the client recognize their own problematic thoughts. In this case the active psychological component to generalized anxiety disorder is an unchallenged or unrecognized thinking pattern that leads to rumination (Ruscio et al., 2015).
In (MacNamara & Proudfit, 2014) is the suggestion that points to the inability on the part of the person with generalized anxiety disorder diagnosis to regulate attention away from unpleasant internal stimuli. This psychological stance would imply that there is a deficit in functions that assist in directing attention when there is a cognitive load that is overwhelming. Further, this study implies that rumination following an event contributes to symptoms of generalized anxiety disorder. The rumination which becomes a pathological behavior was in service to ameliorate stress. It is shown to create a negative feedback loop that is indicative of stress sensitivity for the person with generalized anxiety disorder. The rumination then may have temporarily lessened but did not moderate the anxiety in the stressful situation.
Neurological
The study (Etkin, Prater, Schatzberg, Menon, & Greicius, 2009) points to evidence of neurological issues that support cognitive theories of generalized anxiety disorder. In this study functional magnetic resonance imaging (fMRI) was used to look at the brains of both individuals with and without the diagnosis of generalized anxiety disorder. Results indicated that there were differences identified in the connectivity and function of these two cohorts. In the generalized anxiety disorder sufferers there was an issue with basolateral (BLA) and centromedial (CMA) subregions of the amygdala. In this study the BLA was shown to connect with the medial prefrontal cortex. The CMA was connected to the midbrain, thalamus and cerebellum. The differences between cohorts came about as decreased patterns of connection in the generalized anxiety disorder patients. In these subregions of the brain, the generalized anxiety disorder patients showed greater connectivity between these regions and the executive control center of the brain.
There was evidence that abnormalities existed in the connections between these brain regions and the amygdala. In addition, findings showed issues with connections in the frontoparietal executive center.
The evidence that there are actual neurological underpinnings to generalized anxiety disorder is supported by (Weinberg, Klein, & Hajcak, 2012). The use of measures called error related negativity or (ERN) which point to potentials of erroneous responses to certain stimuli have been linked with issues in the anterior cingulate cortex. The response is such that 50ms after the event, there is a deflection of activity. This marks points in the neural networks that reflect constructs within the brain that show specific attenuation in response to neural networks.
Biochemical
(Chung-Man, Heoung-Keun, & Gwang-Woo, 2015) made a study of the brain neurochemicals associated with generalized anxiety disorder. Some areas of the brain that have been associated with generalized anxiety disorder symptoms have been widely studied. In this study the dorsolateral prefrontal cortex (dlpfc) was measured for metabolite concentrations. The specific markers were the choline/creatine (c/c) and choline/N-acetylaspartate (c/N-a ) ratios in the brains of diagnosed generalized anxiety disorder patients compared to persons who do not have this disorder. After being assessed for symptomology and length of time having the disorder, the study then measured the amounts of these neurochemicals. The relations between the cohorts showed that levels of both c/c and c/N-a were at a much lower ratio in those who suffer generalized anxiety disorder symptoms. As well, the negative symptoms that occurred were negatively correlated with lessened amount of these chemicals. The lower the ratio the greater the symptoms of cognitive dysfunction and heightened anxiety. This study also pointed to recent information that shows that levels of glutamate/ creatine (glu/Cr) in the anterior cingulate cortex was positively correlated with severity of generalized anxiety disorder symptoms.
(Rosnick et al., 2016) showed elevated cortisol levels were associated with decreased serotonin levels in older adults that had been diagnosed with generalized anxiety disorder symptoms. It showed that the reduced levels of serotonin that increased cortisol also affected cognitive decline and was associated with additional medical symptoms
The study (Frampton, 2014) used a pregabalin anxiolytic agent that selectively binds to GABA receptors presynaptically in the brain. It reduces the action potential of calcium channels thus reducing the release of excitatory neurotransmitters such as glutamate and monoamines. These actions show that the reduction of these chemical releases improve symptoms that are associated with generalized anxiety disorder. In this case the argument then can be made that higher levels of glutamate monoamines are part of the biochemical process that are implicated in higher levels of anxiety which is seen in populations that suffer generalized anxiety disorder.
Genetic, environmental and socio-cultural factors
Genetics may play an important role in generalized anxiety disorder. From the (American Psychiatric Association, 2013) the numbers for generalized anxiety disorder inheritance show that one third of the risk of having this problem comes from genetic components. In the article (Guffanti et al., 2016) where the study was based upon populations at high risk for generalized anxiety disorder, the percentage of third generation family members was at the fifty percent mark. This does not show the actual genetics of inheritance but does point to a largely genetic predisposition to being diagnosed with generalized anxiety disorder or generalized anxiety disorder symptoms.
As for environmental and socioeconomic actors, there is a lacunae in the study of this aspect of generalized anxiety disorder. Many of the studies point to other factors but this area is one that would need to be further studied. Though studies like (Rapee, 2012) point to some evidence that parenting style may increase the likelihood of anxiety, even the (American Psychiatric Association, 2013) points to the fact that environmental data is scarce and that no discernable evidence has been provided linking these factors to generalized anxiety disorder diagnosis.
Treatment
Psychopharmacological
Several journal articles discuss the use of both pharmacological and psychotherapeutic interventions in the treatment of generalized anxiety disorder. In the (Montgomery, Nielsen, Poulsen, & Häggström, 2014) study there was an effective response to pharmacologic interventions in populations that suffer depression but are comorbid for generalized anxiety disorder. In this case the studies participants were those who had been treated for depression with selective serotonin reuptake inhibitors (ssri) or serotonin– noradrenaline reuptake inhibitors (snri) but who had been switched to the one of the antidepressants, either vortioxetine or agomelatine. In both cases the symptoms for depression and generalized anxiety disorder were reduced.
In the (Anderson, 2006) supplement for new guidelines for treatment of anxiety disorders, the first line of pharmacotherapy is the use of SSRIs because they are highly effective. The guidelines discuss the use of these medications for treatment periods of at least twelve weeks before their efficacy can be measured must continue. In addition to this advice the specific treatment for patients that have been diagnosed with generalized anxiety disorder is that this continue for at least six months.
Another medication treatment that is discussed in (Anderson, 2006) is the use of long term benzodiazepines in patients who are resistant to the use of SSRI’s. In the case of this medication it is not treated lightly due to the potential adverse side effects and addiction potential. The specific SSRI’s that are recommended for their efficacy in treatment of generalized anxiety disorder are escitalopram, paroxetine and sertraline while other antidepressants like venlafaxine, imipramine and buspirone have also been shown to be effective. For more specifics in drug treatment with generalized anxiety disorder the recommendation is that the approach should be longer term than for other anxiety disorders. The other recommendation is that the use of cognitive behavior therapy should be considered in addition to the use of these medications.
Psychotherapy
One interesting study that supports the use of therapeutic techniques is (Rosnick et al., 2016). This study uses a combination of SSRI’s and cognitive behavioral therapy (CBT). The point was to look at the combination to see how much more effective it would be than to treat with medication alone. The hypothesis was that treatment with CBT would improve the outcomes for reduction of symptoms in generalized anxiety disorder through the reduction of cortisol levels. The specific techniques were relaxation training, cognitive therapy, problem-solving skills, and psychoeducation/self-monitoring. In this study it was noted that there was a statistically significant reduction in cortisol levels with this method in relation to treatment without the CBT.
Another study which was a pilot study to begin possible further research was informative in this matter. In (Khattra et al., 2016) the principle of corrective emotional experience was used, backed by the use of both CBT and Motivational Interviewing (MI) techniques to determine the extent that patients who re-experience early conflicts can challenge and revise negative beliefs. In this case the participants suffered generalized anxiety disorder and were introduced to the two different types of therapy. The CBT contained elements of psychoeducation for anxiety and worry, self-monitoring, progressive muscle relaxation training, discrimination training, cognitive restructuring, behavioral experiments, imagined and in vivo exposure to worry cues, prevention of worry-related behaviors, discussion of sleep strategies, and relapse prevention planning. The MI sessions included techniques which target ambivalence about worry and worry-related behaviors while including the strategies of expressing empathy, rolling with resistance, developing discrepancy, and enhancing self-efficacy. At the time of therapeutic completion there was evidence of recovery from generalized anxiety disorder although treatment with MI appeared more effective at the 12 month follow-up.
One other example is from the study (Aviram, Westra, Constantino, & Antony, 2016). This study also looked at CBT and MI but in a different manner. In this case, persons who had been diagnosed with generalized anxiety disorder were given CBT up to and until they came to an area of resistance. When resistance to treatment appeared, the therapist was trained to implement MI techniques. When there was disagreement in the part of the client with the therapist, clients whose therapists switched to an MI style had better outcomes and less post treatment worry.
Clinical Integration
In my own work with clients who receive a diagnosis under the heading of substance use disorder, there are many stories that substantiate the earlier discussion. One case in particular is that of a client who came to me after attending inpatient treatment. He had been diagnosed with Substance use disorder comorbid for generalized anxiety disorder. Techniques used in SUD treatment vary from CBT and MI to psychoeducation. In many cases the clients who have comorbidity for other disorders are treated by pharmacological means. In the above citation, these techniques have been indicated to treat patients who have been diagnosed with generalized anxiety disorder.
The client was prone to rumination and anxiety. The client had been given buspar to deal with anxiety and to calm rumination. With this medication the client’s rumination and anxiety was brought to a level that was manageable and the client was able to focus on the sessions and gain a foothold in therapeutic treatment. The Client received training in anxiety reduction through mindfulness techniques. The 32 sessions of intensive outpatient dealt with cognitive distortions by disputation techniques and reframing with CBT. When the client began to become defensive and argue the use of MI assisted in self-assessment and acceptance.
With the treatment only lasting a short duration, as much psychoeducation and behavioral training as possible is provided to enhance and improve the limited behavioral repertoire of clients. In this case, the client reported a reduction in symptoms of rumination and anxiety at the exit interview. The client was able to pinpoint a moment when he felt the medication and his understanding of his cognitive distortions had enabled him to feel as if he were getting better.
References
American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders (5 ed.). Arlington, VA: American Psychiatric Publishing.
Anderson, I. (2006). The new guidelines from the British Association for Psychopharmacology for anxiety disorders. International Journal of Psychiatry in Clinical Practice, 10(suppl 3), 1010-1017.
Aviram, A., Westra, H. A., Constantino, M. J., & Antony, M. M. (2016). Responsive management of early resistance in cognitive–behavioral therapy for generalized anxiety disorder. Journal of Consulting And Clinical Psychology, 84(9), 783-794. doi:10.1037/ccp0000100
Chung-Man, M., Heoung-Keun, K., & Gwang-Woo, J. (2015). Metabolic change in the right dorsolateral prefrontal cortex and its correlation with symptom severity in patients with generalized anxiety disorder: Proton magnetic resonance spectroscopy at 3 Tesla. Psychiatry & Clinical Neurosciences, 69(7), 422-430.
Etkin, A., Prater, K. E., Schatzberg, A. F., Menon, V., & Greicius, M. D. (2009). Disrupted amygdalar subregion functional connectivity and evidence of a compensatory network in generalized anxiety disorder. Archives of General Psychiatry, 66(12), 1361-1372. Retrieved from https://doi.org/10.1001/archgenpsychiatry.2009.104
Frampton, J. (2014). A Review of its Use in Adults with Generalized Anxiety Disorder. CNS Drugs, 28(9), 835-854.
Guffanti, G., Gameroff, M. J., Warner, V., Talati, A., Glatt, C. E., Wickramaratne, P., & Weissman, M. M. (2016). Heritability of major depressive and comorbid anxiety disorders in multi-generational families at high risk for depression. American journal of medical genetics, , . doi:10.1002/ajmg.b.32477View/save citation
Khattra, J., Angus, L., Westra, H., Macaulay, C., Moertl, K., & Constantino, M. (2016). Client Perceptions of Corrective Experiences in Cognitive Behavioral Therapy and Motivational Interviewing for Generalized Anxiety Disorder: An Exploratory Pilot Study. Journal of Psychotherapy Integration, , . doi:10.1037/int0000053
Lundervold, D. A., Ament, P. A., Holt, P. S., & Hunt, L. S. (2013). Comparison of younger and older adults’ acceptability of treatment for generalized anxiety disorder co-occurring with Parkinson’s disease. International Journal of Behavioral Consultation and Therapy, 8(2), 20-22. doi:10.1037/h0100971
MacNamara, A., & Proudfit, G. H. (2014). Cognitive load and emotional processing in generalized anxiety disorder: Electrocortical evidence for increased distractibility. Journal of Abnormal Psychology, 123(3), 557-565. doi:10.1037/a0036997
Mayo Clinic Staff. (n.d.). Selective serotonin reuptake inhibitors. Retrieved December 10, 2016, from http://www.mayoclinic.org/diseases-conditions/depression/in-depth/ssris/art-20044825
Mills, S. D., Fox, R. S., Malcarne, V. L., Roesch, S. C., Champagne, B. R., & Sadler, G. R. (2014). The psychometric properties of the Generalized Anxiety Disorder-7 Scale in Hispanic Americans with English or Spanish language preference. Cultural Diversity And Ethnic Minority Psychology, 20(3), 463-468. doi:10.1037/a0036523
Montgomery, S. A., Nielsen, R. Z., Poulsen, L. H., & Häggström, L. (2014). Adults with major depressive disorder with an inadequate response to a single course of selective serotonin reuptake inhibitor or serotonin-noradrenaline reuptake inhibitor treatment switched to vortioxetine or agomelatine. Human Psychopharmacology: Clinical & Experimental, 29(5), .
Penney, A. M., Mazmanian, D., & Rudanycz, C. (2013). Comparing positive and negative beliefs about worry in predicting generalized anxiety disorder symptoms. Canadian Journal of Behavioural Science/Revue Canadienne Des Sciences Du Comportement, 45(1), 34-41. doi:10.1037/a0027623
Rapee, R. M. (2012). Clinical Child Family Psychological. Family Factors in the Development and Management of Anxiety Disorders, 15(69), . doi:doi:10.1007/s10567-011-0106-3
Rosnick, C. B., Wetherell, J. L., White, K. S., Andreescu, C., Dixon, D., & Lenze, E. J. (2016). Cognitive-behavioral therapy augmentation of SSRI reduces cortisol levels in older adults with generalized anxiety disorder: A randomized clinical trial. Journal of Consulting And Clinical Psychology, 84(4), 345-352. doi:10.1037/a0040113
Ruscio, A. M., Gentes, E. L., Jones, J. D., Hallion, L. S., Coleman, E. S., & Swendsen, J. (2015). Rumination predicts heightened responding to stressful life events in major depressive disorder and generalized anxiety disorder. Journal of Abnormal Psychology, 124(1), 17-26. doi:10.1037/abn0000025
Weinberg, A., Klein, D. N., & Hajcak, G. (2012). Increased error-related brain activity distinguishes generalized anxiety disorder with and without comorbid major depressive disorder. Journal of Abnormal Psychology, 121(4), 885-896. doi:10.1037/a0028270
Westra, H. A., Constantino, M. J., & Antony, M. M. (2016). Integrating motivational interviewing with cognitive-behavioral therapy for severe generalized anxiety disorder: An allegiance-controlled randomized clinical trial. Journal of Consulting And Clinical Psychology, 84(9), 768-782. doi:10.1037/ccp0000098
World Health Organization. (2016). The ICD-10 classification of mental and behavioural disorders: Clinical descriptions and diagnostic guidelines (10 ed.). Geneva: World Health Organization. Retrieved from http://apps.who.int/classifications/icd10/browse/2016/en#/F41.1