Pets, Fear and Fireworks: The Fallout and Terrible Consequences of Fear and Anxiety for Our Pets. Part 2, Beyond Fear, Anxiety Disorders

In the first article, I looked at how the ‘fear system’ works as a normal, adaptive neurophysiological network essential for the survival of an organism. In this article, I explore the neuropathology of how the ‘fear system’ goes wrong and the serious consequences this has on the animal’s welfare when it does.

What turns a fear into an anxiety?

Well, there is a simple definition –

An anxiety state is a state that mimics fear in terms of arousal, release of stress hormones etc. BUT it occurs independently of external events.

In other words, anxiety is an internalised state, generated by the brain –

in anticipation of a fearful event THAT MAY NEVER OCCUR (COAPE, 2013).

Here is an everyday example –

If a dog is frightened of something, a big aggressive dog standing in front of him for example, and that dog goes away, the fear goes away too. However, if a dog is anxious about big aggressive dogs, because of a previous unpleasant experience with one, simply returning to the field where he was previously attacked may well induce anxiety, even though the big aggressive dog is not there. The field, the context, has become a conditioned cue to feel anxious (remember what we learned in Part 1 of this article about fear conditioning in the amygdala and the role of the hippocampus).

Anxiety is a maladaptive state that causes the sustained arousal of the Hypothalamic-Pituitary-Adrenal (HPA) axis and the consequent ‘flooding’ of the entire body with ‘stress hormones’, including adrenalinenoradrenaline and cortisol.

Prolonged exposure to cortisol of nerve cells in the prefrontal cortex  and the hippocampus and the is particularly damaging. Damage to nerve cells in these particular brain structures and others is a consistent finding in humans and other animals, including dogs, with depression (Duman, 2004).

So there is a link – chronic, unresolved anxiety leads to depression, which further reduces a dog’s ability to adapt and cope.

Damage to areas of the prefrontal cortex – a key ‘thinking’ part of the brain that modulates the more primitive, limbic responses – compromises its ability to over-ride the amygdala’s ‘reflex’ responses to aversive experiences.

The hippocampus is the part of the brain that consolidates new memories and re-processes previous memories when they are recalled. Damage to the hippocampus by prolonged exposure to stress hormones can lead to an ‘exaggeration’ of the perception of new aversive experiences as it consolidates new memories and re-processes recalled previous related memories before sending them back to the cerebral cortices and the amygdala for storage.

In the first article, we described the 2-pathway processing of sensory information in the brain, the so-called “Difference Between The Quick and the Dead” described by LeDoux, 1996. Figure 1, top shows another version of this pathway. The top of the figure shows the normal SIX-PATHWAY processing of fearful events.

A horsy tail
Anyone who knows anything about horses knows how reactive they are around novelty. There is an infamous cartoon card depicting a horse and rider (you can find it in shops and on the internet) where the captions read –

Rider: “CALM down! What’s so scary about a plastic bag?”
Horse: “It’s PLASTIC and it’s a BAG!”

In the first pathway (Figure 1, top), the amygdala, 2. Emotional Response, when left to get on with its own thing, works very much like an over-reactive horse and triggers the 3. Autonomic Response and the 4. Behavioural and Emotional Response.

In the meantime, in the second pathway (Figure 1, top), the cerebral cortex, 5. Cognitive Response, and the prefrontal cortex, 6. Inhibitory Response, work as the rider, controlling the horse with more sensible, cognitive and goal-directed guidance, which generally involves a great deal of stopping the horse from over-reacting – inhibition.

But there is a twist.

The amygdala has already made its decision before the cerebral cortex and prefrontal cortex are even aware that anything has happened.

The cerebral cortex and prefrontal cortex receive the sensory information from the thalamus, 1. Collection and Distribution, about half a second later. This may not seem like much of a delay, but in relation to an innate, reflexive, hard-wired biological avoidance response, it is a L—O—N—G time.

This explains why BOTH these brain pathways need training – like a muscle – in order that they learn to work together in an adaptive and sensible way. This is the foundation of ‘stress immunisation’ in puppies where, along with the socialisation part, they are exposed to as many experiences as possible at a very early age, WHILE THESE PARTS OF THE BRAIN ARE STILL MATURING and WHILE THE AMYGDALA’S FEAR RESPONSES ARE NOT YET FULLY FUNCTIONAL.

This brain-training goes on, of course, throughout a dog’s life and how reactive an individual dog may be is a product of his genetics (‘temperament’) and his previous experiences (good and bad). When a dog experiences fireworks and is frightened of them, these TWO-PATHWAYS in his brain are being trained again.

 In chronic, unmanaged anxiety states, the final stages of sensory processing – 5. Cognitive Response and 6. Inhibitory Response – are shut down, as shown in the bottom image of Figure 1. In, effect, the primitive, hard-wired limbic response is left in control (see the DID YOU KNOW box at the end of this article for more information about these neural circuits).
These mechanisms are involved in the development of post-traumatic stress disorder (PTSD) (Goswami et al., 2013).


Thus, a vicious cycle is created that further exacerbates the dog’s ongoing development of anxiety and depression (see Figure 2).

Prolonged exposure to stress hormones has additional far-reaching effects all over the body damaging other organs and tissues causing increased blood pressure, stroke, heart attacks, diabetes, suppression of the immune system and susceptibility to disease, suppression of the inflammatory system and delayed wound healing etc.

What, exactly, is depression?

Depression is a mood, or affective disorder (an affect is a psychological term that refers to emotional feeling states such as sad, happy, angry, frightened and so on). In humans the affective disorders are a group of related mental illnesses characterised by disordered feelings. All through our lives we go through times when we feel fed up and depressed, but the affective disorders are much more severe and much more prolonged and they are characterised by the patient feeling that they no longer have control over their own circumstances and emotional state. Like anxiety disorders, affective disorders are hugely important and have been well studied as an illness in humans with an estimated 20% (one in five) of us suffering from one in our lifetimes (Marneros, 2007).

We don’t have statistics for dogs because it is difficult to study (you can’t ask a dog how he feels), but we know it exists because it has been experimentally induced in the laboratory and in its extreme form we know it as learned helplessness (Hajszan et al., 2009; Peterson et al., 1993), where dogs will simply give up with loss of appetite, weight loss, animals become passive, immobile, unresponsive to training, unresponsive to contact and stimulation, non-aggressive when provoked etc. These dogs also show the tell-tale signs of brain damage described above. In using the term ‘depression’ in dogs, we should be mindful that we are referring to the known damage to the brain along with the observed behavioural and likely emotional changes. We are not making a direct comparison with the many forms of depression documented for humans.

Anyone working with dogs think this is not relevant to them because it’s ‘too human’?

Think again.

Most of what we now know about anxiety and depression has been learned from studies of animal models, including primates, rodents and dogs. Much of this research would not be allowed today because it would never get past an ethics committee, and quite rightly so – some of the work done was frankly abhorrent. We have nonetheless gained a great deal of valuable information and understanding that can help us in treating our dogs today, and we owe it to the lives of the animals that were used in some of this original research not to waste it.


If you are working with dogs as a trainer or a behaviourist, look out for the ones with fear-related behaviour problems. Look at Figure 3; is this Springer Spaniel just bored or could she be suffering from a separation problem? Be vigilant and identify the subtle changes in body language and general demeanour. Question the owners about changes they may have noticed to their dog’s behaviour around the home and on walks. If you can pick these things up early and deal with them you can prevent or mitigate the damaging consequences of chronic anxiety states described in this article.




Fear Conditioning and Aversive Training Methods

When dogs are trained using aversive, punishment-based methods, for example with an electric shock collar, if the dog’s natural fight-flight response is invoked, then the SIX-PATHWAY processing of ALL incoming stimuli are likely to be short-circuited, with stages 5. Cognitive Response and 6. Inhibitory Response, being inhibited or even shut down (see Figure 1, bottom image).

In effect, the trainer is expecting the dog to learn and perform with only ‘half his brain’ functioning normally! What the dog is actually learning is avoidance behaviours.

The consequences of using shock collars to train dogs is discussed in another blog HERE.



© copyright Robert Falconer-Taylor, 2017

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Images used in this article
1. Schematic of the brain’s 2-pathway sensory processing. Copyright © COAPE, 2017.
2. Schematic of how the brain processes sensory information. Copyright © COAPE, 2017.
3. Anxiety in a Springer Spaniel. Copyright © Robert Falconer-Taylor, 2013.


Available with the publication of the final part of this 4-part series of articles.