Social Contact Eases Neuropathic Pain

Social Contact Eases Neuropathic Pain

They say a friend in need is a friend indeed.  And when it comes to chronic pain, that conventional wisdom isn’t far off the mark.

A new animal study out of Ohio State shows that companionship and social contact can reduce some of the pain associated with nerve damage — which may lead to a greater understanding of neuropathic pain.

In the study, mice that were paired off with a cage mate showed lower pain responses and fewer signs of inflammation in their nervous system after nerve surgery than did isolated mice.

The social contact also appeared to have a beneficial effect when the mice experienced stress before the surgery, suggesting both physical and psychological benefits from the interaction.

The mice were subjected to a specific kind of nerve-related pain called allodynia, which is a withdrawal response to a stimulus that normally wouldn’t elicit a response. In this case, it was a light touch to the paw.

“If they were alone and had stress, the animals had increased inflammation and allodynia behavior,” said Adam Hinzey, a graduate student in neuroscience at Ohio State University and lead author of the study. “If the mice had a social partner, both allodynia and inflammation were reduced.”

“A better understanding of social interaction’s beneficial effects could lead to new therapies for this type of pain.”

Researchers spent a week studying two groups of mice. One group was paired with a single cage mate while the other mice were kept socially isolated. For three days during that week, some mice were exposed to brief stress while others were not.

They then performed a nerve surgery, producing sensations that mimic neuropathic pain on one group of mice, and a fake procedure that didn’t involve the nerves on the control group. After determining a baseline response to the light touch of the paw, researchers tested the behavior of the mice for one week after the surgery.

The study found that mice that had cage mates had less inflammation and neuropathic pain.

They discovered that the mice which lived with a social partner, regardless of stress level, required a higher level of force before they showed a withdrawal response of the paw, compared to isolated mice that were more responsive to a lighter touch.

“Animals that were both stressed and isolated maintained a lower threshold – less force was needed to elicit a paw withdrawal response.  Animals that were pair housed and not stressed withstood a significantly greater amount of force applied before they showed a paw withdrawal response,” said Hinzey.  “Within animals that were stressed, pairing was able to increase the threshold required to see a withdrawal response.”

Researchers also looked at the animals’ brain and spinal cord tissue for the gene activity of two proteins that are typically elevated in response to both injury and stress, and serve as markers for inflammation.

Compared to the control group that received the fake procedure, isolated mice with nerve damage had much higher levels of gene expression in their brain and spinal cord tissue. There was also a significant decrease in gene activity in the spinal cords of non-stressed animals compared to the mice that were stressed.

“We believe that socially isolated individuals are physiologically different from socially paired individuals, and that this difference seems to be related to inflammation,” said Courtney DeVries, professor of neuroscience at Ohio State and principal investigator on this work.

“These data showed very nicely that the social environment is influencing not just behavior but really the physiological response to the nerve injury.”

More than 20 million Americans suffer from peripheral neuropathy, a nagging nerve pain characterized by a loss of feeling in the toes, feet, legs, hands and arms that often includes a persistent burning, tingling or prickling sensation. Caused by disorders such as diabetes and rheumatoid arthritis, few reliable treatments are available.

The findings of the study were released at the annual meeting of the Society for Neuroscience in New Orleans.

Authored by: Richard Lenti