Brain and Anxiety

Fear is an emotion that triggers a response in the brain when there is imminent danger, real or imagined.

This can lead to an automatic response: a fight, flight or freeze response. Fear is an innate emotion that warns of danger in time, but it can become a conditioned, learned emotion.


Research shows that approximately 70% of people fight or flee when faced with danger. 15% of people are able to inhibit these fear responses and respond rationally. They are able, for example, to assist with evacuations in the event of a disaster. 15% of people freeze and can no longer do anything at all.

During such an anxiety attack, there is a split second when the heart rate initially drops and the person stands very still, hyper alert, with all senses open to make a decision (parasympathetic response: brake on the system).


Goosebumps, hair standing on end, big eyes

Immediately after that split second, the heart rate increases and the body prepares for the action of flight or fight
(sympathetic response = action of the system).
The hairs stand on end (goosebumps), the muscles are tensed, the senses become sharper, the pupils dilate and the ears open wide through small muscles. Because the pituitary gland produces endorphins, the body does not feel much pain.
Once the danger has passed, more endorphins and dopamine are produced to restore the balance.


Switching flexibly

It is important that a person can switch flexibly between the parasympathetic response (brake) and the sympathetic response (action), in order to deal with the normal dangers in life.

Remember the importance of fleeing from fire or oncoming traffic in time. This automatic response to fear can be trained a bit, think of snipers who, as it were, put themselves in a 'dead' position (the parasympathetic brake on the nervous system) with a slowed heart rate in order to observe better.


The more fear, the more brain connections in the fear system

The more often someone has had negative experiences with strong feelings, the more brain connections are created in the fear network.
People with these experiences are more likely to freeze in a fearful situation and then flee. People who have experienced frightening things as children have stronger reactions of freezing and can no longer act properly.


People with a tendency towards aggression and people with more testosterone than normal will more quickly get over that moment of rigidity and start fighting.
That is why it is very bad for children and adults to cause them severe anxiety, not even during a Halloween setting, a hazing or a youth camp, for example.


Pituitary gland, hormones and adrenal glands

In case of anxiety, a signal goes from the pituitary gland to the adrenal glands where stress hormones such as adrenaline and cortisol are produced.
Too much cortisol in the blood and chronic stress have a proven negative impact on the body and in particular on the immune system, on heart blood vessels and this can lead to shrinkage of the
hippocampus and other brain structures.


In the group of people who freeze and flee, more cortisol is produced.
People who fight and face danger have a higher testosterone level. This applies to both women and men.


Thalamus, prefrontal cortex, amygdala, hippocampus

  • The thalamus regulates consciousness and vigilance in the event of fright or fear.
  • The prefrontal lobe regulates awareness of how to act in the event of fright or fear.
  • The amygdala is the emotion center of fear.
  • The hippocampus is the memory center of fear.


Incoming information that comes in during stress or anxiety can be processed in the brain via two pathways.

Via a short route (unconscious) and a long (conscious) route.
The thalamus quickly provides information to the amygdala on the short route or via the long route to the cerebral cortex of the frontal lobe. There it is analyzed what needs to be done and only then is the information sent to the amygdala.
The fear memory is stored in the amygdala. In people with aggression, the amygdala appeared to be enlarged.


A second fear system runs through the intermediate station of the
hippocampus involved in learned emotions. This area is important for memory and associations. Traumatic memories are, as it were, burned in there under the influence of adrenaline.

The hippocampus and the amygdala can influence each other. They can thus evoke or strengthen an emotion. Based on a fearful memory, the hippocampus can alert the amygdala to be ready to fight or flee.


People with damage to the hippocampus often cannot identify what they are afraid of, but they do feel an unconscious reaction of fear.


Fear memory and fear association

It is useful for the body to store fearful memories in order to quickly recognize and avoid danger in the future. The fear memory or emotional memory is a different system than conscious memory. The hormone norepinephrine appears to play an important role in the formation of this fear or emotional memory.


When fear is followed by a painful stimulus, fear associations are formed. Every neutral fact can be added to the fear memory through fear associations.
Without the person being aware of it, the body can "remember something" later on and this can cause a fear response. Fear is therefore stored and can arise at any time. As a result, someone can react more quickly with fear.



Brain activity can be measured with an MRI scan. When the frontal lobe is influenced a little with magnetic impulses, you see that people become more impulsive. Automatic tendencies can then be controlled less well.

People with brain damage in the frontal lobe also have reduced control over emotions.

People with elevated testosterone, which is more commonly seen in psychopaths, showed less frontal lobe control of emotion. The emotions are then inhibited in the amygdala. These people are therefore more impulsive and more likely to be aggressive.


J.E. Le Doux.The Emotional Brain: The Mysterious Underpinnings of Emotional Life, 1996, Simon & Schuster, 1998 Touchstone edition: ISBN 0-684-83659-9
Maha L, Szabuniewicz C and Fiocco A.J. .Can anxiety damage the brain? Curr Opin Psychiatry 2016, 29:56 – 63
McEwen BS, Stellar E. Stress and the individual. Mechanisms leading to disease. Arch Intern Med 1993; 153:2093 – 2101.

Taylor CT, Aupperle RL, Flagan T, et al. Neural correlates of a computerized attention modification program in anxious subjects. Soc Cogn Affect Neurosci 2014; 9:1379 – 1387. 131.

Lucassen PJ., Pruessner J, Sousa N., Almeida OFX, Van Dam AM, Rajkowska G, Swaab DF, Czéhcorresponding B. Neuropathology of stress Acta Neuropathol. 2014; 127(1): 109–135.

R.M. Visser The neural dynamics of fear memory