More Than You Ever Wanted to Know About
Pain Management
Do animals feel pain?
Looking at the hardware, the anatomy, and the physiology, it is hard to make a case that they do not feel pain. Animals have the exact same nerves, same spinal cord, and same structures inside the brain as we do. All these nerves and things work in the very same way that our nerves and things work. And observationally, animals react to what we would consider painful stimuli in much the same was as we do.
Once we accept the fact that animals feel pain
and that they feel pain in a manner very similar to the way we feel pain, the question immediately arises as to what we can do about that pain. The short answer is, "Lots." There are a variety of drugs and techniques available to help ease the pain our furry companions feel.
Some of what follows is pretty technical. Every practitioner has certain "hobbies" within the scope of their practice. These are areas that the practitioner finds particularly interesting, and about which he or she develops a high degree of skill and expertise. I personally (Dr. Nield, that is), find pain management very interesting, and have over the years spent a lot of time studying and researching this fascinating field. While I can't claim to be a specialist in pain management (it is not ethical to claim to be a specialist in something unless you are board certified in that field), I do believe that we do an excellent job of managing pain at Sunnyside Veterinary Clinic, and that we have some things to offer that you may not find just anywhere else.
Pain is a sensation we feel when our body is damaged
That is how nature lets us know that there is a problem. In this respect, pain has a physiologic function, because it leads us to avoid the thi ng that caused the pain (pulling away from a hot stove), to protect the injured part while it heals (not walking on a broken leg), and to even begin treatment of a wound (in the case of dogs, licking a wound).
Pain starts with receptors at the ends of nerves called nociceptors. The word itself comes from the same roots as the words noxious and receptor. Nociceptors are activated by bad things, like burns, cuts, blunt trauma, stretching, chemical reactions etc. They are also activated by pressure, touch, and other normal stimuli. Some areas, like the skin, are well-supplied with nociceptors. Other areas, like the liver, have very few nociceptors. There are separate nociceptors for heat, stretching, touch, and trauma. Here, mechanical, chemical, and thermal energy causes the nociceptors to be activated. The chemical stimuli can come from either outside sources, such as an acid burn, or internal sources. When tissues are injured, say by a bruise or a cut, they release a number of substances. Histamine, prostaglandins, bradykinins, and other compounds associated with inflammation are released which act directly on the nociceptors.
A particularly interesting aspect of nociceptor function is peripheral sensitization.Sensory endings in inflamed tissue display enhanced sensitivity to stimulation so that usually non-painful stimuli become painful (allodynia) and the perception of painful stimuli becomes more intense (hyperalgesia). Various inflammatory mediators like histamine, bradykinins, and prostaglandins have been shown to cause sensitization in this way. Thus, the sensory endings of nociceptors are modulated and, through them, the perception of pain.
Once nociceptors are activated, they send signals up the nerves towards the brain
There are different kinds of nerves. There are fast "A-delta" nerves, which rapidly carry the initial sensation sharp pain, slow "C" nerves which carry the secondary dull, throbbing pain sensations, and very sensitive "A-beta," or tactile nerves, which have a lower threshold of stimulation and which are responsible for our sense of touch.
The first stop is the spinal cord.
Here, a complex process of switching, routing, and modulation occurs. The spinal cord is the first place the body tries to make sense out of all the varied and assorted signals the injured area sends it. All the different signals from all the different types of nociceptors and all the different types of nerve fibers converge for the first time in the spinal cord.
Sometimes good things happen to the pain signal in the spinal cord, sometimes bad things happen to the pain signal.
In a certain region of the spinal cord, called the dorsal horn, a lot of bad things can happen to a pain signal. Through a process called "dorsal horn wind-up," a form of central sensitization, a relatively mild pain stimulus can be amplified and modulated such that it becomes exaggerated. Long after the initial cause of the pain has subsided, dorsal horn wind-up can result in prolonged and exaggerated pain.
The next stop for the pain signal is the brain
Once the modified pain signal reaches the brain it is processed further. Things like fear and anxiety are allowed to modify the pain sensation. All of the pre-processed signals from all of the various nerves are processed into the perception of pain.
This final result is the sum of all the pre-processing that goes on in the nociceptors, nerves and spinal cord combined with a lot of post-processing that occurs in the brain itself. In some cases, all the pain signals bouncing around can lead to a generalized hyperexcitability called central sensitization, which can lead to excessive pain.
One of the most important concepts to master about pain management is the idea that our nerves are not just wires that carries pain signals from point A to the computer-like brain, which then impartially processes the pain signal.
On the contrary, our nervous system processes pain a lot like a community processes a disaster. Several different people may see an accident happen (the nociceptors), but each may report it in a different way. Some people are more excitable than others, and some may give an inflated report (peripheral sensitization). They then pass the initial report along to other people at the coffee shop (the spinal cord), and there may be considerable discussion with some wild speculation thrown in.
Sometimes things get out of hand (dorsal horn wind-up), and a exaggerated message emerges. The coffee shop people pass their information as they perceive it along to the newspaper (the brain), where the editorial committe tries to process it. Like most committees, sometimes excitable people can dominate the process (central sensitization), leading to a response that may or may not be appropriate for the original accident.
Because of the complexities of the nervous system
with all its nociceptors, nerve fibers, dorsal horns, and brain synapses, there are a lot of points at which we can control and modify the pain signals. Let's start at the very beginning and evaluate how various drugs can modify the pain process.
The nociceptors are where the pain response begins.
Several classes of drugs act directly on the nociceptors to modify the pain response. Non-Steroidal Anti-Inflammatory Drugs, or NSAID's for short, are one such class. Aspirin, ibuprofen, meloxicam, and carprofen are all NSAID's. They act to reduce the amount of prostaglandins that are released by injury, thus reducing their direct nociceptor stimulation and their peripheral sensitization.
A second class of drugs that act directly on the nociceptors are the local anesthetics. These are drugs like lidocaine, bupivicaine, and novocaine. They are injected at the site of pain, and they totally block the nociceptors temporarily, just like when we go to the dentist's and he injects novocaine into our gums. Blocking the pain, even temporarily, can have a great effect even after the local anesthetics wear off because that prevents the spinal cord and brain from getting over-zealous in thier modification of the pain response.
A third class of drugs that can act on the nociceptor level are the opioids. They will be discussed in depth later, but there are some opioid receptors present in the periphery, and they can have a local effect there.