As I’ve been reading Dr. Stephen Porges’ work on the autonomic nervous system, I’ve become increasingly interested in the relationship between behavioral medication and the nervous system of the dog.

This is not an argument against medication. Behavioral medications can be extremely valuable, particularly when a dog is experiencing so much fear or anxiety that learning, rest, exploration, and relationship-building are difficult. Veterinary behavior medicine recognizes medications such as fluoxetine, trazodone, gabapentin, and clonidine as useful tools for different behavioral and situational problems in dogs.

But medication does more than change what we can see on the outside. It changes physiology.

Porges describes the nervous system as continuously receiving information from both the external environment and the internal organs. His concept of neuroception refers to the nervous system's ability to detect cues of safety and threat without conscious awareness. Importantly, this process includes information coming from inside the body as well as from the environment.

This raises an interesting question for anyone working with an anxious dog:

What happens to the nervous system when we pharmacologically change the signals it is receiving or the way it responds to those signals—and then remove the medication?

The answer depends very much on the medication.

Some drugs primarily reduce acute physiological arousal. Clonidine, for example, is an alpha-2 adrenergic agonist that reduces sympathetic nervous-system activity. When certain centrally acting alpha-2 drugs are stopped abruptly after ongoing use, a phenomenon known as rebound sympathetic activation can occur. In medicine, clonidine withdrawal is associated with increased sympathetic activity and a rise in catecholamines.

This is a genuine example of a nervous system temporarily overshooting in the opposite direction after a pharmacological brake is removed.

That is different, however, from simply saying that a dog's anxiety has "come back."

If a medication makes a fearful dog less reactive and the behavior returns when the medication is discontinued, there are at least two possibilities. The underlying anxiety may simply still be present, meaning the medication was successfully managing the symptoms without eliminating their cause. Or, depending on the medication, there may be an actual withdrawal or rebound phenomenon. These are not the same thing.

This distinction is particularly important because the medications commonly used in canine behavior work through very different mechanisms. Fluoxetine is an SSRI used as a longer-term behavioral medication, while trazodone and gabapentin may be used for more immediate or situational anxiety, and clonidine can be used as a situational medication as well.

So I think a more useful question than "Does this medication calm the dog?" is:

What is the medication changing, and what happens to the nervous system when that influence is reduced or removed?

There is another important concept here: interoception—the nervous system's processing of information about the body's internal condition. Porges describes visceral feedback as an important part of the information available to the nervous system and argues that physiological state can influence how an organism responds to the world around it.

This does not mean that medication simply "turns up" the signals coming from the organs when it is discontinued. That would be an oversimplification, and there is not sufficient evidence to make that claim about dogs in general.

A more scientifically cautious way to describe the possibility is that changes in medication can alter autonomic and interoceptive signaling, and some medications can produce physiological rebound or withdrawal when reduced or stopped.

For dogs, this distinction matters.

A dog who becomes more reactive after medication is discontinued may not necessarily have become "dependent" on the medication. The original anxiety may have returned. There may be an adjustment period. There may be a drug-specific withdrawal effect. Or there may be a combination of these factors.

This is also why medication should not be viewed as a substitute for helping a dog develop greater behavioral flexibility. Medication can create enough physiological stability for a dog to sleep, explore, learn, recover from stress, and participate in behavior modification. Veterinary guidance commonly recommends combining behavioral medication with an appropriate behavior-modification plan.

For me, this brings us back to one of the most interesting ideas in Porges' work: physiological state affects the range of behaviors available to an animal.

The goal is not simply to make a dog look calmer, the larger goal is to help the dog develop the capacity to experience the world with greater flexibility—to notice something unfamiliar, recover from it, explore, engage socially, and return to a more settled state.

Medication may be one tool that helps make that possible. Relationship, environment, appropriate behavioral work, adequate rest, and opportunities for exploration are others.

And when medication is eventually reduced, the question is not simply, 

"Is the behavior back?"

Instead we might ask: 

"What has actually changed in the dog's capacity to experience and navigate the world?"

That is a much more interesting question—and, I think, a much more useful one.

 

 

Photo credit: Elina Volkova