Electromagnetic field stimulation potentiates endogenous myelin repair by recruiting subventricular neural stem cells in an experimental model of white matter demyelination.

Electromagnetic fields (EMFs) may affect the endogenous neural stem cells within the brain. The aim of this study was to assess the effects of EMFs on the process of toxin-induced demyelination and subsequent remyelination. Demyelination was induced using local injection of lysophosphatidylcholine within the corpus callosum of adult female Sprague-Dawley rats. EMFs (60 Hz; 0.7 mT) were applied for 2 h twice a day for 7, 14, or 28 days postlesion. BrdU labeling and immunostaining against nestin, myelin basic protein (MBP), and BrdU were used for assessing the amount of neural stem cells within the tissue, remyelination patterns, and tracing of proliferating cells, respectively. EMFs significantly reduced the extent of demyelinated area and increased the level of MBP staining within the lesion area on days 14 and 28 postlesion. EMFs also increased the number of BrdU- and nestin-positive cells within the area between SVZ and lesion as observed on days 7 and 14 postlesion. It seems that EMF potentiates proliferation and migration of neural stem cells and enhances the repair of myelin in the context of demyelinating conditions.

Transcranial magnetic stimulation shows impaired transcallosal inhibition in Marchiafava-Bignami syndrome.

A case of Marchiafava-Bignami (MB) syndrome with selective callosal involvement was evaluated by clinical examination and magnetic resonance imaging (MRI) in the acute phase and 6 months after the onset of symptoms; at the same time, the corticospinally and transcallosally mediated effects elicited by transcranial magnetic stimulation (TMS) were investigated. The first MRI study showed the presence of extensive abnormal signal intensity throughout the entire corpus callosum. After high-dose corticosteroid administration her symptoms rapidly resolved, in parallel with the reversion of MRI changes, except for severe cognitive impairment. Follow-up TMS examination revealed persistent transcallosal inhibition (TI) abnormalities. This report indicates that the measurement of TI during the course of MB syndrome is useful for evaluating functional changes to the corpus callosum, including their evaluation with time and after treatment and for elucidating the pathophysiology of MB syndrome.

Radiation-induced apoptosis of oligodendrocytes in the adult rat optic chiasm.

OBJECTIVES: The present study characterized glial cell injury provoked in adult rat chiasm within 24 hours after a single, high-dose irradiation of 20 Gy. METHODS: All chiasmal glial cells in a section were counted, and the percentage of TUNEL-positive glial cells exhibiting apoptotic morphology was defined as the apoptotic rate. RESULTS: Numbers of apoptotic cells increased significantly (p<0.0001) from 3 to 8 hours after exposure, but returned to baseline levels by 24 hours. Little evidence of apoptosis was observed in non-irradiated chiasms. Similar patterns of increase in apoptotic rate were observed in the genu of the corpus callosum, but the extent was significantly lower (p=0.047) in the optic chiasm, with a maximal rate of 1.9%. Immunohistochemically, apoptotic cells were positive for CNP, a marker for oligodendrocytes. DISCUSSION: These data indicate that chiasmal irradiation induces limited, but significant apoptotic depletion of the oligodendroglial population, and may participate in the development of radiation-induced optic neuropathy.