chronic pain

A peptide found in bull ant venom closely resembles a hormone of its primary predator, triggering hypersensitivity and making subsequent bites even more painful than the ones that came before.

Study finds that, contrary to what other research has found, a popular meditation course does not appear to alter brain structure.

The University of Guelph neuroscientist is scoping out the brain regions and genes that change as a consequence of pain that lasts for months or even years.

Human data and experiments in mice challenge the common use of anti-inflammatory drugs to treat pain.

The Smith-Kettlewell Eye Research Institute scientist developed Botox for medicinal use.

Abnormal sympathetic neuron growth leads to simultaneous activation of clusters of sensory neurons, causing the difficult-to-treat sensation.

Taking inspiration from her PhD research, Ana Moreno formed a company where scientists use CRISPR to treat chronic pain

Prolonged exposure to morphine triggers cells in the spine to release signaling molecules that increase pain sensitivity and dull the relief of the drug. Blocking this activity could improve pain management.

Patients in a small trial said their chronic pain improved an average of 90 percent over the course of 15 days, but returned shortly after the electrical stimulation sessions ended.

When researchers injected mice with antibodies from fibromyalgia patients, the animals developed symptoms of the disease—suggesting that it may be controlled by the immune system, not the nervous system.

After resigning from the University of New England last year, Geoffrey Bove continues to study the effects of massage on rats in a facility he set up in his house.

The findings could represent a novel mechanism for relieving inflammatory pain.

Genetic material from the chikungunya virus remains in mouse cells after infection and may be linked to later joint pain.

The glia seem to make up part of a newly described sensory organ, the discoverers suggest.

Men’s pain tolerance decreases when exposed to a setting where they’ve previously had a painful experience.

Researchers silence pain neurons in the mouse spinal cord with injections of botulinum toxins modified to bind to the neurons’ receptors.

Immune-like cells in the central nervous system are now recognized as key participants in the creation and maintenance of persistent pain.

The race to develop analgesic drugs that inhibit sodium channel Na_V1.7 is revealing a complex sensory role for the protein.