Now, here’s where it gets interesting. Over the years, many studies have looked at people with fibromyalgia and found evidence of small fiber neuropathy. Some research suggests that as many as 30% of people diagnosed with fibromyalgia actually meet the criteria for small fiber neuropathy. One study using skin biopsies found neuropathy in 41% of fibromyalgia patients! Conditions like complex regional pain syndrome and other types of widespread, unexplained pain also show signs of this nerve involvement.
Instead of thinking of fibromyalgia as just a muscle or joint problem, it’s becoming clearer that the issue might actually be rooted in how the brain and spinal cord process pain signals. Let’s break down how pain signals travel.
Pain starts at the edges of your body, with nerve cells (neurons) picking up a sensation. These signals are sent along nerves to the spinal cord, and then up to the brain. The brain is where these signals are interpreted as pain. If this communication pathway gets messed up, it can lead to chronic pain conditions, including neuropathic pain.
One key player in sending pain signals up the spinal cord is a chemical messenger called glutamate. Glutamate activates specific receivers on nerve cells called NMDA receptors. When these are activated, the signal travels to certain parts of the brain that process pain. This is like turning up the volume on pain signals – it’s called pronociception.
On the flip side, other parts of the brain send signals down the spinal cord to turn the volume down on pain. This is called antinociception, or anti-pain signaling. It’s like a natural volume control for pain.
The Role of the Dorsal Root Ganglia
A critical area involved in this pain processing is located along the spinal cord and is called the dorsal root ganglia (DRG). Problems in the DRG have been linked to small fiber neuropathy and, potentially, fibromyalgia pain.
What can happen is that after an initial trigger – maybe an injury, an infection, or even a nutritional deficiency – the nerve cells in the DRG can start to change. They can grow extra branches, a process called sprouting. This sprouting makes the DRG become overly sensitive to chemicals from the sympathetic nervous system, like catecholamines. The result? Neurons start firing too much, a state known as hyperexcitability.
This is why stress can sometimes make fibromyalgia pain worse. When your sympathetic nervous system (your fight-or-flight response) is activated, it can trigger these hypersensitive sensory neurons to fire. To make matters worse, this problem of overactive pain signals going up to the brain is often combined with a reduction in the brain’s ability to send those dampening signals down. So, you get a double whammy: more pain signals coming in and less ability to turn them off. This can lead to chronic pain, even when there’s no obvious ongoing injury or stimulus.
