Generalized Anxiety Disorder: Pharmacological Treatment

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Table of Contents

Biological Theories
Best Theory
Pharmacological Treatments
Mechanism of Action
Possible Side Effects
Interactions and Contraindications
References

Biological Theories

Jeremys presenting symptoms that meet the DSM-V criteria for generalized anxiety disorder (GAD) (Slee et al., 2019). According to its etiology, higher DNA methylation of corticotropin-releasing factor increases GAD risk and severity as do reduced resting-state functional connectivity between the amygdala and prefrontal cortex and overactivation of the sympathetic nervous system due to stimuli (Slee et al., 2019, p. 771). Thus, epigenetic mechanisms, limbic structures, and hypervigilance cause GAD.

Best Theory

The evidence from genetics, neurobiology, and psychophysiology implicates neurobiological factors in GAD development. Affected serotonin neurotransmission is associated with heightened feelings of worry and fear even in the absence of a threat (Slee et al., 2019). Thus, the neurobiological theory offers the best explanation for GAD etiology. The physiological states and behavioral components seen in GAD patients result from neurological differences between anxious and non-anxious cohorts.

Pharmacological Treatments

Antidepressants from different classes are indicated as first-line therapy for GAD. According to Slee et al. (2019), selective serotonin reuptake inhibitors (SSRIs), such as Lexapro, are effective medications for treating anxiety. Another class of anti-anxiety drugs, benzodiazepines, are used in GAD treatment when administered orally or parenterally. However, the risk of dependency is high with these medications; hence, they are not used as a first-line treatment.

Mechanism of Action

SSRIs target serotonergic neurons that occur in cortical and limbic areas. Their binding to the serotonin transporter (receptors) prevents the reuptake of neurotransmitters by the presynaptic neuron (Slee et al., 2019). Therefore, serotonin is not reabsorbed sooner but rather accumulates, inducing anxiolytic effects. In contrast, benzodiazepines target gamma-aminobutyric acid (GABA) receptors that are excited in an anxious state to induce anti-anxiety effects in GAD patients.

Possible Side Effects

Jitteriness, nausea, and migraines are common adverse effects of SSRIs. Patients treated with these drugs may also experience restlessness, low energy, poor appetite, and sexual dysfunction (Slee et al., 2019). They may manifest many behavioral symptoms such as confusion and agitation, drowsiness, and hallucinations. On the other hand, the adverse effects associated with benzodiazepine treatment include fatigue, vertigo, slow reaction time, and impaired cognitive functioning.

Interactions and Contraindications

SSRIs interact with non-steroidal anti-inflammatory drugs (NSAIDS) and blood thinners, reducing their effectiveness. Their interaction also increases the risk of bleeding in users. SSRIs are contraindicated in bipolar disorder, hemophilia, diabetes, and epilepsy (Slee et al., 2019). On the other hand, benzodiazepines are not suitable for patients with sleep apnea, chronic obstructive pulmonary disease, and bronchitis. These medications mostly interact with phenothiazines, antidepressants, and barbiturates.

References

Slee, A., Nazareth, I., Bondaronek, P., Liu, Y., Cheng, Z., & Freemantle, N. (2019).

Pharmacological treatments for generalised anxiety disorder: A systematic review and network meta-analysis.The Lancet, 393(10173), 768-777. Web.

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