Brain plasticity is often touted as a miracle cure, but it does have a dark side. Addiction, for example, occurs as a result of neuroplasticity within the brain’s reward system. Now, an animal study by a team of researchers from Stanford University shows that a newly described form of plasticity likely contributes to the progression of epilepsy.
The new study, led by Juliet Knowles, was performed on an inbred strain of rats that grow to develop spontaneous ”absence” seizures (which involve a lapse in consciousness) similar to those in humans.
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The results, published in Nature Neuroscience, show that the electrical activity associated with epileptic seizures increased both the proliferation of immature oligodendrocytes and the number of mature oligodendrocytes in the corpus callosum, leading to abnormal overproduction of myelin that in turn promoted the progression of epilepsy.
It is, however, too soon to directly extrapolate the findings to epilepsy in humans. Epilepsy takes various forms in humans, which differ in cause, age of onset, and location and severity of seizures, and so the role of myelin plasticity is also likely to differ between each form. Nevertheless, further investigation of maladaptive myelination may eventually lead to novel strategies for treating epilepsy and other neurological conditions.
