Using a new brain scanning technology, neuroscientists at Massachusetts General Hospital in Boston have produced dramatic images showing how glial cells – cells derived from the immune system that live in the nervous system – get activated in chronic pain patients. The technology should not only help diagnose pain, but boost research into the novel idea of using an antibiotic and other anti-glial drugs to treat back pain. (Citation: Brain, March, 2015.)

When pain signals from nerve cells land on glial cells, the glia pump out chemical signals that then land on other nerve cells, ramping up transmission of pain signals to the brain. Hundreds of animal studies have shown that blocking glial activation reduces pain, but human studies have lagged behind.

The new technique, a merger of PET (positron emission tomography) and MRI (magnetic resonance imaging) showed clear evidence of glial activation in patients with low back pain. Neuroscientist Marco Loggia’s team compared nine patients with chronic back pain with nine matched controls without pain. In the pain patients but not the controls, the brain scans showed elevated levels of a protein called TSPO, a marker of glial activation. Strikingly, levels of TSPO were higher not just in the thalamus but in the somatosensory cortex, specifically in parts of the “homunculus” (a map-like representation of the body) corresponding to the lumbar spine and the leg, exactly where the pain patients hurt. (Curiously, the more intense the pain reported by the patients, the lower the levels of TSPO, perhaps because the increase in TSPO during the inflammatory response may itself have an anti-inflammatory component.)

The new technique expands the booming field of imaging to study pain. At Boston’s Children’s Hospital, neurobiology and neurologist David Borsook has used imaging to show brain changes in chronic pain patients responding to treatment.

The new study may also spur research into the idea of treating chronic pain with the antibiotic minocycline, which has the side effect of blocking glial activation. “It’s time to be more aggressive in this,” Loggia says. Sean Mackey of Stanford and University of Colorado neuroscientist Linda Watkins are also pursing the use of a form of naltrexone (an opioid blocker) to damp down glial cells.

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