Tooth pain as well as pain in the eyes and ears tends to be more disruptive and emotionally draining than pain elsewhere in the body. Now, researchers at Duke University have found how the brain’s wiring makes people suffer more from head and face pain, triggering the senses as well as the emotions.
Sensory neurons that serve the head and face are wired directly into one of the brain’s principal emotional signaling hubs. Sensory neurons elsewhere in the body also are connected to this hub, but only indirectly. These findings may lead to more effective treatments for pain mediated by the craniofacial nerve, such as chronic headaches and neuropathic face pain.
“Usually doctors focus on treating the sensation of pain, but this shows that we really need to treat the emotional aspects of pain as well,” said Fan Wang, PhD, a professor of neurobiology and cell biology at Duke and senior author of the study.
Pain signals from the head and those from the body are carried to the brain by two different groups of sensory neurons. It is possible that neurons from the head are simply more sensitive to pain than neurons from the body. But differences in sensitivity would not explain the greater fear and emotional suffering that patients experience in response to head-face pain than body pain, Wang said.
Personal accounts of greater fear and suffering are backed up by functional magnetic resonance imaging, which shows greater activity in the amygdala—a region of the brain involved in emotional experiences—in response to head pain than in response to body pain.
“There has been this observation in human studies that pain in the head and face seems to activate the emotional system more extensively,” said Wang. “But the underlying mechanisms remained unclear.”
To examine the neural circuitry underlying the two types of pain, the researchers tracked brain activity in mice after irritating either a paw or the face. They found that irritating the face led to higher activity in the brain’s parabrachial nucleus (PBL), a region that is directly wired into the brain’s instinctive and emotional centers. Next, they used proprietary technology to pinpoint the sources of neurons that caused the elevated PBL activity.
“It was a eureka moment because the body neurons only have this indirect pathway to the PBL, whereas the head and face neurons, in addition to this indirect pathway, also have a direct input,” said Wang. “This could explain why you have stronger activation in the amygdala and the brain’s emotional centers from head and face pain.”
Further experiments showed that activating this pathway prompted face pain, while silencing the pathway reduced it.
“We have the first biological explanation for why this type of pain can be so much more emotionally taxing than others,” said Wolfgang Liedtke, MD, PhD, a professor of neurology at the Duke University Medical Center and co-author of the study. “This will open the door not only toward not only a more profound understanding of chronic head and face pain, but also toward translating this insight into treatments that will benefit people.”
Chronic head and face pain such as cluster headaches and trigeminal neuralgia can become so severe that patients seek surgical solutions, including severing the known neural pathways that carry pain signals from the head and face to the hindbrain. But a substantial number of patients continue to suffer, even after these invasive measures. Triggering the neural pathway identified here, Liedtke said, can be a new approach in developing treatments for this pain.
The study, “A Craniofacial-Specific Monosynaptic Circuit Enables Heightened Affective Pain,” was published by Nature Neuroscience.
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