Brain and fear

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.
In itself, fear is an innate emotion that can warn for danger, but it can become a conditioned, learned emotion.


Research shows that approximately 70% of people fight or flee from 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. The last 15% of people freeze and can no longer do anything at all. 

 

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

 

Goosebumps, hair on end, big eyes

Immediately afterwards, 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 feels less pain.
Once the danger has passed, more endorphins and dopamine are produced in the body to restore balance.

 

Flexible switching

It is important that a person can switch flexibly between the parasympathetic response (brake) and 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 be able 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 fearful things as children have stronger freeze reactions and then are unable to act properly.
People with aggression or with more testosterone will get over that moment of freezing more quickly and start fighting.
That is why it is absolutely not good for children or adults to be made anxious or frightened, not even during the setting of Halloween, student initiation 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. In particular on the immune system, on the heart and blood vessels and this can lead to shrinkage of the hippocampus.

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

 

Thalamus, prefrontal cortex, amygdala and 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 during stress and anxiety can be processed in the brain via two pathways. Via a short (unconscious) route and a long (conscious) route.


The thalamus quickly provides information to the short route
amygdala 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 also 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 brain 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. Therefore, 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 anyone being aware of it, the body can later "remember something" and this can cause a fear response.
Fear is stored and can arise at any time. A person can therefore react more quickly with fear.

 

Impulsiveness

Brain activity can be measured with an MRI scan. During a scientific study, magnetic impulses were used to determine the
frontal lobe slightly influenced by the examiner. The research immediately showed that people became more impulsive. Automatic tendencies could then be controlled less well.
People with brain damage in the frontal lobe also have a brain injury
reduced control over emotion due to brain damage.
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. They were therefore more impulsive and more aggressive.

 

Neural pathways can change

Neural pathways connect relatively distant parts of the brain. Each path is associated with a certain action or behavior.
New thoughts and skills actually pave new paths.
Repetition and practice strengthen these pathways and form new habits.
Old paths are then used less and weaken over time.
Every time we think, feel or do something we STRENGTHEN a neural connection. That requires a lot of repetition and practice.
If fear tells you something that is not the truth or real, put the truth against it! Repeat that reality and truth.

 

The vagus nerve or 10th cranial nerve (X) can help calm the nervous system and the overloaded brain because this nerve controls the parasympathetic nervous system (REST!). We explain the anatomy and function on the Nervous System page.


We explain the application of how you can learn to calm your body on the Rest in your nervous system page. A good respiratory therapist or Heartmath therapist can teach you to lower your heart rate and calm your brain through breathing exercises. This causes the stress hormones in the body to drop, which is good for the body.

 

However, every therapist must realize that people with brain damage use more brain areas to express emotion. To shape their thoughts. To adjust behavior. Knowledge of the specific damaged brain areas, or what difficulties someone specifically has due to the injury, are requirements for this therapy to be successful.

 

The preconditions are: bring peace. slow down the pace.
Adapt to the daily circumstances of the person with brain injury. As a therapist, communicate a little slower and clearly, without subordinate clauses. Pay attention to your own facial expressions as a therapist. A friendly face will convey peace. See, among other things, the page
Communicating with someone with a brain injury.

 

 

Resources

 

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 memoryhttp://dare.uva.nl/search?metis.record.id=501016http://dare.uva.nl/search?metis.record.id=501016

 https://pure.uva.nl/ws/files/2714598/167826_09_Summary_Samenvatting.pdf

Albert Kok imageCollege door prof. psychopathologie Karin Roelofs. Universiteit van Nederland.