Animal Research Points to Possible Treatment for Severe Chronic Pain

Research published recently in the Journal of Clinical Investigation suggests that severe chronic pain might be treated by selectively deleting specific nerve cells that convey the pain through the nervous system.

A research team led by the National Institutes of Health in April reported that a series of experiments in rats demonstrated that a drug called resiniferatoxin could be injected in the ganglia of rats and selectively kill some cells while allowing the rats to maintain normal motor and sensory function. The researchers then followed up by using the technique to treat dogs suffering from chronic pain.

The researchers used eight dogs who had been brought to veterinary hospitals with severe pain from arthritis and cancer. The dogs were injected with resiniferatoxin to kill the neurons responsible for the sensation of chronic pain felt by the dogs. According to a press release from NIH on the study,

So effective was the treatment in eight dogs severely affected by osteroarthritis, cancer-related pain, or both, all eventually became more active and later walked with slight or no limps. Just as importantly, none showed any adverse side effects from their treatments, their temperaments were improved, and their need for other pain-controlling medications was eliminated or greatly reduced.

In addition, the pain relief the dogs experienced did not diminish as their disease progressed. Dr. Michael Iadarola said in a prepared statement,

We were very encouraged to see a long-term therapeutic benefit that did not diminish with the progression of the disease. When a cancer progresses, you often have to increase the dose of conventional pain medications, such as opiate analgesics, which can produce alterations of consciousness, activity level, and other severe side effects that can impair overall quality of life.


Animal studies show promise treating severe chronic pain. Press Release, National Institute of Dental and Craniofacial Research, May 3, 2004.

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