# The Neurological Basis of Anxiety



## David Baxter PhD (Dec 20, 2017)

*The Neurological Basis of Anxiety*
by Viatcheslav Wlassoff, PhD, _Brain Blogger_
December 20, 2017

A person suffering from an anxiety disorder experiences  neurology-based changes in mood and bodily functions that are discussed  in more detail in this article.

 As with anxiety, various personality traits and emotional responses  are by-products of the interaction between our genetic coding and  environmental influences. Our genes make us more receptive to some  specific stimuli and play a role in developing the resilience to some  other stimuli. Our brain is a plastic organ. Thus, the role of  environmental factors in its development and casting cannot be negated.

 Fear and stress are normal defensive reactions to threats that help  our body to deal with challenges more efficiently. Anxiety is different  from fear in that it is a set of emotional and somatic reactions to a  future threat that _may or may not be_ realistic. To some extent,  having anxiety is a normal human reaction. However,  if it continues  for a prolonged period, it may have an adverse effect on our daily life  and health.

 In the state of anxiety, worrying about the future makes it difficult  to concentrate and leads to irritability. Somatic symptoms like  palpation, sweating, and gastrointestinal changes are also common in  this state. Anxiety is considered as a disorder if such symptoms persist  over a period of six or more months.

 Anxiety disorders are most prevalent among people with psychiatric  disorders, affecting around 10% of the population at any given time.  Nonetheless, only a small number of those suffering from anxiety  disorders seek treatment. This can be partially explained by the  difficulties in identifying the condition. General anxiety disorder,  panic disorder, specific phobias, and social anxiety are some of the  most common types of anxiety disorders.

*What makes a person vulnerable to anxiety disorders?*
 The hereditary nature of various forms of anxiety disorders has been  established through clinical and observational studies. Multiple studies  have demonstrated that a person is at 3?5 times greater risk of  developing anxiety disorders if such a condition is found among  first-degree relatives. The importance of familial clustering in anxiety  has been demonstrated by a number of twin studies. Other internal  factors like certain personality traits also make a person more  vulnerable to developing anxiety disorders.

 Apart from internal factors, environmental factors may also make some  people more anxious. These factors include exposure to stressful  condition, drug or alcohol use, parenting style, and stressful life  events.

*Neuroanatomy of stress and anxiety*
 Higher cognitive centers in our brain are located in the prefrontal  cortex. They are involved in thinking, planning, and social behavior.  From an evolutionary perspective, the prefrontal cortex is the ?newer?  part of the brain that helps us to keep our emotional responses in  check.

 Most of the emotion processing takes place in more ancient parts of  the cortex. These anatomical brain structures are collectively called  the ?limbic system?. One fundamental structure in the limbic system is  the hippocampus that plays a vital role in the stress response and  regulation of the hypothalamic?pituitary?adrenal (HPA) axis. Both  hippocampal growth and neurogenesis play an essential role in the  development of resiliency towards stress and anxiety.

 But perhaps the most crucial part of the limbic system that plays a  central role in the regulation of emotions is the amygdala. The amygdala  is central to the formation of fear and anxiety-related memory and has  been shown to be hyperactive in anxiety disorders. It is well connected  with other brain structures like the hippocampus, thalamus, and  hypothalamus.

 Apart from anatomical changes, it is essential to understand that  brain functionality or communication between various brain centers and  networks takes place through neurotransmitters. In the case of emotional  responses, gamma-aminobutyric acid (GABA) is known to have an  inhibitory effect on emotions, while glutamate has an excitatory effect.  The roles of serotonin, dopamine, and norepinephrine are also well  documented in the pathogenesis of various emotional states. Other  neurotransmitters that may play a role in the pathogenesis of anxiety  disorders are cholecystokinin (CCK), galanin (Gal), neuropeptide Y  (NPY), oxytocin (OT), vasopressin (AVP), and corticotrophin-releasing  factor.

*Neuroanatomical changes in stress*
 Most anxiety disorder cases develop in childhood, where the long-term  and repetitive experience of anxiety leads to changes in specific brain  structures that can be observed using neuroimaging. fMRI studies on  generalized anxiety disorder (GAD) have shown a higher level of activity  in the ventrolateral prefrontal cortex. Furthermore, a significant  level of activity is seen in the amygdala, especially when a person is  told to focus on his or her stress, as well changes in the cingular  cortex and insular cortex.

 During adolescence, there is an acceleration in the physical growth,  along with changes in behavior, cognition, and emotional control. The  development of the body during this period may result in permanent  changes in various brain areas that can be implicated in the development  of psychiatric disorders in adult life.

 During adolescence, it might be easier to remodel various brain  structures with the help of cognitive behavioral therapy or other  modalities than in adults. Meanwhile, in adults, various therapeutic  agents can be used to alter the biochemical structure of the brain.

 For patients with anxiety disorders, selective serotonin reuptake  inhibitors (SSRIs) and serotonin-norepinephrine reuptake inhibitors  (SNRIs) are often prescribed as the first line treatment. Other drugs  that can be used to treat various anxiety disorders include monoamine  oxidase inhibitors, tricyclic antidepressants, and benzodiazepines.

 Despite the immense progress in our understanding of neuroanatomy and  neuroendocrinology, not all cases of anxiety can currently be treated.  However, the latest research on the subject has improved the selection  of drugs available for various anxiety disorders. For instance,  benzodiazepines are known to be more efficient in the treatment of panic  disorders than GAD.

 As neuroimaging technologies continue to evolve, a better  understanding of the neurobiology of anxiety is bound to influence the  way we treat anxiety and other related disorders.

*References*


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 Bandelow, B., & Michaelis, S. (2015). Epidemiology of anxiety disorders in the 21st century. _Dialogues in Clinical Neuroscience_, _17_(3), 327?335. PMCID: PMC4610617 
 Bystritsky, A., Khalsa, S. S., Cameron, M. E., & Schiffman, J.  (2013). Current diagnosis and treatment of anxiety disorders. _Pharmacy and Therapeutics_, _38_(1), 30?57. PMCID: PMC3628173 
 Martin, E. I., Ressler, K. J., Binder, E., & Nemeroff, C. B.  (2009). The neurobiology of anxiety disorders: brain imaging, genetics,  and psychoneuroendocrinology. _The Psychiatric Clinics of North America_, _32_(3), 549?575. doi:10.1016/j.psc.2009.05.004 
 Miguel-Hidalgo, J. J. (2013). Brain structural and functional changes in adolescents with psychiatric disorders. _International Journal of Adolescent Medicine and Health_, _25_(3), 245?256. doi:10.1515/ijamh-2013-0058 
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 Ravindran, L. N., & Stein, M. B. (2010). The pharmacologic treatment of anxiety disorders: a review of progress. _The Journal of Clinical Psychiatry_, _71_(7), 839?854. doi:10.4088/JCP.10r06218blu


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