Capsaicin cream

Capsaicin cream, ointment, and lotion (also called capsicum cream) claim to reduce all sorts of pain, from headaches to phantom limb pain, to trigeminal facial neuralgia. In fact here's a list of pain that capsaicin is claimed to help from about.com

Osteoarthritis
Post-surgical neuropathic pain
Back pain
Pain due to diabetic neuropathy
Joint pain
Nerve Pain
Phantom pain after amputation
Bursitis
Post-herpetic neuralgia
Pruritis (itching)
Fibromyalgia
Rheumatoid arthritis
Muscle pain

There are also some anti-aging wrinkle creams containing capsaicin on the market, but those are discussed on that page, not here.

Can these claims really be true? Well, in fact they can, in theory, by two seperate mechanisms. If you haven't already, read the capsaicin pain page to find out first how it causes pain, then you will understand better the info here on how it reduces pain.

Here's the gist of the next paragraph describing the first mechanism that can reduce pain cause it's sort of complicated. TRPV1 lets in calcium. The calcium then signals the cell to take the receptor off the membrane and to close the channel so that the cell won't die. The neuron is then less likely to signal to the spinal cord that there is pain, since it is a pain signaling neuron.

The first mechanism is fast. Remember TRPV1, the capsaicin receptor and calcium channel? Well, when it is open it lets in loads of calcium, which depolarizes the cell (lets the voltage across the membrane reach equilibrium). This is how neurons communicate with each other and how you percieve pain, but if prolonged can kill the cell, which is called excitotoxicity. So if there is a prolonged calcium increase (such as when capsaicin binds to TRPV1), the cell uses mechanisms to stop it. One of these is to endocytose the TRPV1 receptor, that is to get it off the cell membrane so that it can't let in extracellular calcium anymore. Another is to close the channel using a negative feedback loop. Calcium binds to a calcium chelator in the cell called calmodulin (CaM) which is a cofactor for many enzymes. CaM, when bound with calcium let in by TRPV1, can bind directly to the TRPV1 receptor and close the channel. CaM also activates several kinases, which phosphorylate the channel so that it closes (Mandadi et al. 2006). The net effect of all this is that less calcium is let in which makes it less likely that the neuron will fire, telling the dorsal root ganglion and brain that you're in pain.

This is the same mechanism your body uses to habituate to hot water. You know how if you put your hand in really hot water you pull it back immediately, but if you force yourself to keep it there for a few seconds it is not as painful? Remember that TRPV1 is a noxious heat receptor, and that capsaicin is an agonist to it, all the mechanisms which apply for heat also apply for capsaicin. Capsaicin cream, ointment, and lotion are quite simply just a heating pad that doesn't get cold. Heating pads help for lots of pain, and this is why capsaicin cream does too.

Ok, the second mechanism and arguably the most important is slow, habituation by the central nervous system. The brain responds to change. Not the same annoying droning over and over. As I write this birds are chirping outside, but it wasn't until I was writing this paragraph looking for an example of habituation that I noticed it. My brain tunes it out because it's the same thing over and over. The same happens for any repetitive signal. When capsaicin ointment is applied, it causes a constant signal to be sent to the central nervous system by the pain neurons. After awhile, the brain starts to ignore, or habituate to, the pain neurons. Guess what that means, capsaicin lotion makes your brain ignore the neurons that are sensitive to capsaicin, which are the pain neurons. Most of the habituation mechanism involves depletion of the neurotransmitters that the sensory neurons use to communicate with the dorsal root ganglion and the rest of the central nervous system. One of the main neurotransmitters which signals pain, Substance P, is released from pain sensing neurons into the dorsal root ganglion. Capsaicin facilitates this release, and if capsaicin is continuously applied, the cell runs out of Substance P to signal with, therefore giving you a higher pain threshold, and higher threshold for noxious heat (Yaksh, et al. 1979).