The Neurobiology of Anxiety

This post explains the neurobiology of anxiety in very simple terms.  It covers some of the basic brain structures and functions as well as the neurotransmitters involved in the experience of anxiety.  Just understanding how anxiety operates on a physiological basis can be reassuring to those who are suffering from it.  For one thing, understanding anxiety in physiological terms is helpful because it becomes clear that what you are experiencing is very real. It is not something in your imagination or that you should expect yourself to be able to simply use your will to make go away.

The experience of anxiety primarily arises from the limbic system of the brain (often called the emotional brain). In simple terms, the limbic system is comprised of the thalamus, the hypothalamus, the hippocampus and the amygdala.  Each part of the limbic system plays a role in generating anxiety, but it begins in the thalamus which is a relay station for incoming information about the external world. The thalamus takes information from our senses (sight, sound, touch, taste, and smell) and assesses it for possible danger.  This information then travels through the brain down what is often referred to metaphorically as either the low road or the high road.

The low road refers to circuitry involving the amygdala which is the early warning or alarm station of the brain.  This part of the brain operates unconsciously.  It is an automatic response to what is perceived as immediate danger. The high road circuitry involves another part of the brain referred to as the cortex, the part of the brain that is needed for conscious thought, the formulation of ideas and the attribution of meaning.  The part of the cortex which is significant to anxiety is the prefrontal cortex which processes information, maintains conscious attention, forms behavioral repsonses and makes meaning of sensory experience.

When danger is perceived by either road, the brain mobilizes it’s response to the stress.  This response is often described as “fight, flight or freeze”.  It involves the hypothalamus-pituitary-adrenal  (HPA) axis which is the brain system that initiates the stress response to prepare the body to respond to a stressor. The hypothalamus initiates the response by releasing a peptide called corticotropin release factor to the pituitary gland.  The pituitary in turn releases adrenocorticotropin to the adrenal gland which releases adrenalin and cortisol.  The HPA axis starts the sympathetic nervous system arousal which results in increased heart rate and respiration and the redirection of blood flow.  This response also uses up neurochemicals such as serotonin, dopamine and norepinephrine.
Thus when the stress response is initiated, it causes changes in neurochemicals, breathing, blood flow and motor responses.  These responses are meant to be short term reactions to danger in the environment, but they can be initiated not only by actual dangers but also by thoughts of danger and particularly thoughts that have been associated with danger in the past.  When an experience has been associated with danger in the past, even the anticipation or thought of that experience can trigger the stress responses described above.  One of the greatest factors determining whether a stress response will be initiated is the meaning attributed to the potentially threatening experience.  When stressors (be they internal or external) are constant, the stress response described above functions continuously and anxiety results.

A goal of symptom management for anxiety is to find ways to trigger the parasympathetic nervous system to slow the physiological arousal associated with the stress response described above.  Another goal is to prevent the stress response from being triggered using cognitive control and physical self management techniques such as exercise and meditation.

 

 

Anxiety Series Part Four: The Neurobiology of Anxiety

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