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Na+/myo-inositol cotransporter has been shown to protect cells from the perturbing effects of hypertonic stress by the accumulation of myo-inositol. Here we report a regulatory mechanism for the cotransporter. Induction of myo-inositol cotransporter mRNA was observed after exposure to veratridine, a voltage-gated sodium channel opener. The veratridine-elicited induction was inhibited when Na+ was eliminated from the bath, although calcium chelation failed to modify the gene expression. Veratridine evoked an accumulation of Na+ in the cells, which paralleled the abundance of the mRNA. These results strongly suggested that an increase in Na+ influx due to sodium channel opening affected transcription of the cotransporter gene. Activity of the myo-inositol cotransporter was also up-regulated after veratridine exposure. To clarify the possible roles of myo-inositol accumulation under veratridine exposure, we next examined the neurotoxic effects of veratridine when myo-inositol uptake was blocked. Neither 30 μM veratridine nor 500 μM 2-O,C-methylene myo-inositol, a competitive inhibitor of myo-inositol, elicited apparent cytotoxicity. However, a combination of these agents markedly increased cytotoxicity in culture, suggesting that an adequate amount of myo-inositol was necessary when the cells were stimulated with veratridine. [ABSTRACT FROM AUTHOR]

Hemifacial spasms (HFS) are usually caused by vascular compression on the extra-axial facial nerve. In this case, we concluded that an intra-axial brainstem cavernous angioma with a venous angioma diagnosed by MRI must have been responsible for HFS, because no other possible causes were found during intraoperative observations. [ABSTRACT FROM AUTHOR]

Abstract: Backgroud: Difficulty for distal exposure of the ICA is sometimes encountered during CEA. A carotid shunt is used to maintain sufficient cerebral blood flow during CEA but requires fixative materials, such as a string or a metallic ring, which often restrict the operative field, especially that of the distal ICA. Methods: Here, we describe a novel technique for carotid shunt fixation using a unique fixative device in CEA. In the method presented here, the carotid shunt is fixed with an inflated balloon and a conventional vascular tourniquet proximally, but distal fixation is achieved using a Sugita''s fenestrated clip that catches the mid portion of the carotid shunt and surrounding tissue. Results and Conclusion: The device prevents the distal carotid shunt slipping out of the distal ICA. The present method allows mobilization of the shunt position during CEA and facilitates far-distal exposure of the ICA. [Copyright &y& Elsevier]

Objectives Phantom limb pain is neuropathic pain after amputation of a limb and partial or complete deafferentation such as brachial plexus root avulsion. The underlying cause of this pain has been attributed to maladaptive plasticity of the sensorimotor cortex. It has been suggested that experimental reorganization would affect pain, especially if it results in functional restoration. We tested the hypothesis that restoration of hand motor function using a brain–machine interface (BMI) based on magnetoencephalographic (MEG) signals will normalize maladapted cortical representation and relieve pain. Methods This study included 10 phantom limb patients (9 brachial plexus root avulsion and 1 amputee). MEG signals during movements of the phantom hand or intact hand were used to train the decoder inferring movements of each hand. The robotic hand was controlled by the decoder. Patients controlled the robotic hand by moving the phantom hand. The training effects were compared among trainings with the phantom decoder, real hand decoder, and random decoder in a randomized cross-over trial. Results BMI training with the phantom decoder increased the decoding accuracy of phantom hand movements and pain. In contrast, BMI training with the intact hand decoder reduced accuracy and pain. Discussion It was suggested that BMI training to modulate the motor representation of phantom hand controlled pain. The sensorimotor cortical plasticity might induce pain. Conclusions and Significance Phantom limb pain was controlled by BMI training to induce sensorimotor cortical plasticity. [ABSTRACT FROM AUTHOR]

We present a 9-year-old girl with an endodermal cyst of the oculomotor nerve in the left interpeduncular cistern, who had a history of left ptosis. We suggest that a cyst localized at the exit of the oculomotor nerve from the midbrain associated with oculomotor palsy may suggest this rare entity. [ABSTRACT FROM AUTHOR]

Background Vertebrobasilar artery entrapment resulting from a clivus fracture is rare. The entrapped lesions are not radiographically depicted precisely because they are only identified by autopsy or completely occluded. In addition, no changes in the features have been revealed clearly because radiologic examinations were performed only in the acute stage. Case Description We report a case of traumatic entrapment of the vertebral artery depicted precisely by a three-dimensional angiographic study in the subacute stage, presenting the serial changes in the morphologic features and a review of the published cases. Conclusion It is necessary to manage vertebrobasilar artery entrapment cautiously because it is suggested that the entrapped lesion is accompanied by arterial dissection. [ABSTRACT FROM AUTHOR]

A letter to editor commenting on study regarding concentration of local free fatty acids in body during carotid artery stenting is presented.

A letter to the editor is presented in response to the article regarding the significance of difference between continuous and paroxysmal patterns of pain in the assessment of pain after brachial plexus injury.

A 74-year-old man showed a spastic gait and myelopathy in both the hands. Computed tomography revealed an OPLL on C3 and C4, bony spurs on the dorsal side of C4-C6, and an OYL on C3 and C4. We scheduled a two-stage decompression for both the OPLL and OYL. First, we performed laminectomy on the C3-C6 segments and resected the OYL. We did not observe any dural tear or CSF leakage in the dura. The patient's neurological symptoms improved. After the laminectomy, his myelopathy recurred. Postoperative MRI showed a spinal cord herniation. We had the C3/4 anterior cervical disectomy and fusion as we planned. In addition, we performed a surgery to repair the damaged dura mater at the site of spinal cord herniation at the same second surgery. The integrity of the arachnoid membrane was preserved. The patient's myelopathy gradually improved. There have been no reports on postoperative neurological deterioration caused by spinal cord herniation associated with a dural defect at the laminectomy site, without dural tear in the surgery after the resection of a posteriorly located cervical OYL. The possibility of a dural defect in OYL cases should be considered when planning a laminectomy for the resection of the OYL. [ABSTRACT FROM AUTHOR]