Author: Donald Doherty

People with central pain syndrome often experience pain without cessation. The cause is from damage to brain tissue or brain abnormalities that the person was born with. More than 50% of people with spinal cord injuries and 30% of people with multiple sclerosis experience central pain syndrome.

The research team that recently published the paper “Abnormal Activity of Primary Somatosensory Cortex in Central Pain Syndrome” in the September 2010 issue of Journal of Neurophysiology uses a rat model of the central pain syndrome to investigate possible mechanisms underlying this devastating problem.

A previous study by this group has shown that the zona incerta, a group of inhibitory neurons in the brain, sends less signals to the posterior thalamic nucleus in rats with central pain syndrome. The result, known as dis-inhibition or the removing of inhibition of the posterior thalamic nucleus by the zona incerta, results in increased spontaneous and sensory evoked activity in the thalamus.

In this study, the team looked at activity in the primary somatosensory cortex which is a major target of the posterior thalamic nucleus. They hypothesized that they would see higher spontaneous and sensory evoked activity in rats with central pain syndrome. Indeed, they saw spontaneous activity increase by 350% and sensory evoked activity increase up to 220% in the primary somatosensory cortex of rats with central pain syndrome.

Data from this study add to a body of data suggesting that the primary somatosensory cortex is at least partly responsible for the excruciating pain experienced by central pain syndrome patients. Understanding the brain mechanisms underlying the syndrome may lead to therapies for these patients. For example, a study that used hypnotic suggestions to alter perceived pain intensity produced correlative changes in primary somatosensory cortex activity.

Recent research published in the September 3, 2010 issue of Science shows that social cliques (clustered ties with a high degree of separation between clusters) are more effective at spreading behaviors across social networks than less tightly knit social groups that provide shortcuts across social space.

This finding is surprising since you might think that behavior would spread faster the broader the individual contacts across social space. On the other hand, a social clique is natural for a human so perhaps it’s not surprising that it’s optimal for spreading behavior (assuming that spreading new behaviors as rapidly as possible improves the chances for survival).

The paper, titled “The Spread of Behavior in an Online Social Network Experiment,” also reported that adoption of a behavior became increasingly likely the second, third, and fourth time an individual received a recommendation from a social network friend. More recommendations didn’t affect adoption.

Wouldn’t it be interesting to see if those with really large clusters of social network friends (for example, individuals with thousands of Facebook friends) move out of the optimal social clique configuration. Perhaps collecting as many social network friends as you can get changes recommendations into noise?

It seems reasonable to assume that two minds working to solve a problem are better than one. Recent research published in a paper titled “Optimally Interacting Minds” in the August 27, 2010 issue of Science calls this assumption into question.

The research showed when two people with similar abilities collaborate through communication that indeed they do perform better than either one would on their own. However, when the two people have different abilities the collaboration performs worse than the best performer would on their own.

This suggests that you should not try to solve a problem as a team with a person with lesser or better abilities than you have. If you’re working on a problem team up with someone with similar abilities. Otherwise, delegate the problem to someone with better abilities.