Anxiety is an emotional reaction, a sense of apprehension that in many ways resembles fear but builds up more slowly and lasts longer.

When the senses detect a threat, like a sudden noise, a frightening sight, or an unpleasant feeling, the information goes to the brain by two different pathways.

The short pathway . When startled, the brain automatically sends an emergency message to its fear center, the amygdala.

Once activated, the amygdala sends out the equivalent of a news report to alert other brain structures.

The result is the classic fear response: moist palms, quickened heartbeat, increased blood pressure and an adrenaline spike. All this happens before the mind is conscious of having actually touched or seen anything.

The long pathway. Only after the fear response is activated, does the conscious mind start acting.

Rather than traveling directly to the amygdala some sensory information takes a longer route, stopping first at the thalamus, and then the cortex; the raw data streaming is analyzed to see whether a fear response is required. If it is, the cortex signals the amygdala, and the body stays on high alert.

When a stressful event occurs, the amygdala (brain on alert),activates a series of changes in the body’s chemicals (neurotransmitters) and hormones that trigger anxiety (anxiety and/or fear as a physiological response to a ‘stressor’).

The body’s sympathetic nervous system, responsible for heart rate and breathing, moves to a higher gear. The heart beats faster, blood pressure rises and the lungs hyperventilate. Sweat flows more freely, and even the nerve endings on the skin are activated, creating goose bumps.

The senses become hyper-alert, becoming acutely aware of the surroundings and looking for potential new dangers.

Adrenaline enters the muscles, preparing the body to fight or flee. The brain stops thinking about pleasant things, and turns to identifying potential threats. To prevent energy being wasted on digestion, the body sometimes responds by freeing the digestive tract through involuntary vomiting, urination or defecation.

Responding to signals coming from the hypothalamus and pituitary glands, the adrenal glands deliver high levels of the stress hormone cortisol. Too much cortisol will cause the cells in the hippocampus to become short circuited, making it difficult to organize the memory of the trauma or stressful experience.

Memories can no longer be placed in context and therefore become fragmented.

All animals appear to feel anxiety, indeed without it, survival would be difficult for all of us.

Anxiety becomes a serious problem only when it lasts too long. Anxiety disorder, is any anxiety which lasts so long as to interfere with everyday life. It is relatively common, and can range from very specific phobias to generalized anxiety disorder.

Panic disorder is a recurrent sudden attack of acute anxiety that comes on and reaches its highest point within about ten minutes.

People often panic in familiar surroundings, such as a crowded elevator.

Anxiety is a problem only if it lasts appreciably longer than the immediate threat.

At times there is an evident cause, but occasionally it is difficult to understand why apprehensive feelings go on so long.

When anxiety lasts longer than the threat and becomes a permanent condition, unnecessarily and is annoying for the wellbeing of the subject, it becomes a real pathology.

Clinically, it is characterized by the following:

Sigmund Freud recognized two main forms of anxiety; one, more biological in nature and the other, more dependent on psychological factors.

• anxiety can be hereditary: some people seem to be born worriers.
• imaging diagnostics of the brain can reveal differences in the way patients who suffer from anxiety disorders respond to threats
• due to a shortcut, in our brain’s information-processing system, we can react to danger even before we become consciously aware of it
• the cause of an anxiety disorder may not be the threat that activates it but a failure in the mechanism that keeps anxiety from escaping control.

Scientists have taught laboratory rats to fear everything from buzzers to lights, by giving them electrical shocks whenever they hear a buzzer or see a light.

The rats quickly learn to fear the stimulus even when the shock is absent.

Scientists have gradually mapped fear as it travels through the rodent’s brain. When the rat feels the stress (electrical shock), its senses immediately send a message to the central portion of its brain, where the stimulus activates two neural pathways.

One of these pathways is a relatively long, tortuous route through the cerebral cortex (brain). The other route is a kind of emergency shortcut that quickly reaches an oval shaped cluster of cells: the amygdala.

The amygdala can rapidly “turn on” almost every system in the body enabling it to fight back or run as fast as it can. It’s designed for speed, not accuracy. While the amygdala is telling the body what to do, it also fires up a nearby group of neurons called the hippocampus.

The job of the hippocampus is to help the brain learn and form new memories. The hyppocampus allows the rat to remember where the shock took place and what was happening at the time.

This contextual learning helps the rat to avoid dangerous places in the future. It probably also helps it to distinguish dangerous situations from safer ones.

Meanwhile, the other half of the stress signal reaches the cortex, which confirms that there is a danger present and realizes that this is what is causing pain. Once the initial shock has subsided, the prefrontal cortex of the brain sends a message to the amygdala saying that it’s safe to relax.

It is apparently harder to switch off a stress reaction than to switch it on, which makes excellent sense in terms of survival: it is better to panic unnecessarily than to be too relaxed in the face of a life-threatening danger.

The anxiety response is not necessarily caused by an external threat; rather it may be traced to a breakdown in the mechanism that signals the brain to stop responding.

Anxiety disorders may be caused by an overactive amygdala or an underactive prefrontal cortex.

With advances in technology, researchers have started using Computerized Tomography scans and Magnetic Resonance Imaging (a newer version of traditional X-rays), to understand the subtle changes associated with mental illness and to identify problem areas in many psychiatric disorders.

According to Paul Salkovskis, Professor of Clinical Psychology at University of London, claiming that anxiety disorder is due to a particular area is too simplistic.

Eventually researchers would like to learn more about the roles of nature and nurture (i.e. genes and the environment) in the development of anxiety. Which means answering the question: are people born anxious or do they become anxious following specific life experiences?

Kendler’s found that identical twins were rather more likely than fraternal twins to suffer from generalized anxiety disorder, phobias and panic attacks.

Many claim that the genes determine general vulnerability to anxiety, and that people can be low vulnerable, intermediate-vulnerable, or high vulnerable. But the way people are raised and their life experiences still play a major role.

People with a low genetic vulnerability, for example, could easily develop a fear for flying after surviving a plane crash.

A child, brought up in an insecure atmosphere, will be much more likely to suffer from anxiety than children born into a secure environment.

The links between anxiety and depression are a major issue. Researchers have discovered that depressed adults were often anxious children.

Conversely, many children outgrow anxiety disorders and go on to become well adjusted adults: does anxiety perhaps have some effect the brain, making it more prone to depression later in life?

The amygdala has been seen to be very active in depressed patients, even when during sleep. Twins who share similar anxiety traits tell us that many of the same genes could be involved.

According to some scientists, anxiety and depression share a similar underlying biology (Dennis Charney, Mood and Anxiety Disorders, NIMH, Bethesda).

Some antidepressant like Serotonin Reuptake Inhibitors (SSRI), seem more helpful in treating anxiety than depression. The pathways for reducing anxiety are apparently much harder to reverse than those for increasing it.

But it is wrong to believe that pills alone can normalize human neurochemistry, since they may eliminate the symptoms but not the cause (Lepastier).

If anxiety disorders were purely biological, then psychotherapy would be ineffective. Howeer, even in the short term, allowing the anxious patients to explain their anxiety does afford some relief. which brings us back to the cerebral cortex, where you would expect psychotherapy to work (calming message to the amygdala).

Certain desensitization techniques can also help but their effectiveness also depends on the severity of the trauma.
Reference (Time, August 26, 2002).

Treating anxiety
A number of strategies can help in the treatment of anxiety.

The pharmacological treatment of anxiety is similar to that of depression. We will discuss both in the chapter on ‘depression and ’medication’ .