Scientists have known since the 1800s what happens to a totally crushed peripheral nerve in animals: the damaged axons are broken down in a process called Wallerian degeneration, allowing healthy ones to regrow. But humans rarely suffer complete axonal damage. Instead, axons tend to be partially damaged, causing neuropathic pain — a difficult-to-treat, chronic pain associated with nerve trauma, chemotherapy and diabetes.
Neuropathic pain is chronic pain originating through some malfunction of the nervous system, often triggered by an injury. It causes hypersensitivity to innocuous stimuli and is often extremely debilitating. It doesn’t respond to existing painkillers — even opioids can’t reach it well.
New research in a mouse model, described last week in Cell Reports, deconstructed neuropathic pain and could offer new leads for treating it. The carefully done study showed that two major neuropathic pain symptoms in patients — extreme touch sensitivity and extreme cold sensitivity — operate through separate pathways.
“We think this separation will allow targeted drug-based therapies in the future,” says Michael Costigan, PhD, of the F.M. Kirby Neurobiology Center at Boston Children’s Hospital, who was the study’s senior investigator. “If our results stand experimental scrutiny by others, this will be profoundly important in our overall understanding of neuropathic pain.” …
It’s bad enough that invasive infections are painful. New work suggests that pain is only a means to an end for virulent bacteria: It’s how they suppress our immune system.
Previously, the pain from invasive infections like meningitis, necrotizing fasciitis, urinary tract infections, dental caries and intestinal infections was thought to be due to the body’s immune response, causing the infected tissue to become inflamed and swollen.
Not so, says Boston Children’s Hospital neuro-immunologist Isaac Chiu, PhD. Studying invasive skin infections caused by methicillin-resistant Staphylococcus aureus (MRSA) in live mice, his team’s research demonstrates that the pain is induced by the bacteria themselves, and kicks in well before tissue swelling peaks.
Adding outrage to insult, once the pain-sensing neurons are activated, they suppress the immune system, potentially allowing the bacteria to proliferate, finds the study, published last week in Nature.…
Though autism can respond well to early behavioral interventions, it’s typically not diagnosed in the U.S. until around age 5, when these interventions are less effective. Autism is diagnosed based on a child’s behaviors and language, which take time to develop to the point where clinicians can reliably assess them. What’s really needed is a fast, objective test when a child is much younger, before symptoms even show up.
In the past decade, researchers have chipped away at the problem, linking more than a dozen genetic mutations to autism—from small DNA “spelling” changes to lost or extra copies of a gene or genes (known as copy number variants) to wholesale chromosome abnormalities. Tests have been created, such as the chromosomal microarray test. But together, the known mutations account for, at best, 1 in 5 autism cases among tested patients. …