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.
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