Analysis of youtube as a source of information for peripheral neuropathy.

INTRODUCTION: YouTube is an important resource for patients. No study has evaluated the information on peripheral neuropathy disseminated by YouTube videos. In this study, our aim was to perform a systematic review of information on YouTube regarding peripheral neuropathy. METHODS: The Web site (www.youtube.com) was searched between September 19 and 21, 2014, for the terms "neuropathy," "peripheral neuropathy," "diabetic neuropathy," "neuropathy causes," and "neuropathy treatment." RESULTS: Two hundred videos met the inclusion criteria. Healthcare professionals accounted for almost half of the treatment videos (41 of 92; 44.6%), and most came from chiropractors (18 of 41; 43.9%). Alternative medicine was cited most frequently among the treatment discussions (54 of 145, 37.2%), followed by devices (38 of 145, 26.2%), and pharmacological treatments (23 of 145, 15.9%). CONCLUSIONS: Approximately half of the treatment options discussed in the videos were not evidence-based. Caution should be exercised when YouTube videos are used as a patient resource.

Hypoxia enhances high-voltage-activated calcium currents in rat primary cortical neurons via calcineurin.

Hypoxia regulates neuronal ion channels, sometimes resulting in seizures. We evaluated the effects of brief sustained hypoxia (1% O(2), 4h) on voltage-gated calcium channels (VGCCs) in cultured rat primary cortical neurons. High-voltage activated (HVA) Ca(2+) currents were acquired immediately after hypoxic exposure or after 48h recovery in 95% air/5% CO(2). Maximal Ca(2+) current density increased 1.5-fold immediately after hypoxia, but reverted to baseline after 48h normoxia. This enhancement was primarily due to an increase in L-type VGCC activity, since nimodipine-insensitive residual Ca(2+) currents were unchanged. The half-maximal potentials of activation and steady-state inactivation were unchanged. The calcineurin inhibitors FK-506 (in the recording pipette) or cyclosporine A (during hypoxia) prevented the post-hypoxic increase in HVA Ca(2+) currents, while rapamycin and okadaic acid did not. L-type VGCCs were the source of Ca(2+) for calcineurin activation, as nimodipine during hypoxia prevented post-hypoxic enhancement. Hypoxia transiently potentiated L-type VGCC currents via calcineurin, suggesting a positive feedback loop to amplify neuronal calcium signaling that may contribute to seizure generation.

Ischemia-induced increase in microvascular phosphodiesterase 4D expression in rat hippocampus associated with blood brain barrier permeability: effect of age.

Phosphodiesterase 4D (PDE4D) is one of 16 PDEs expressed in cerebral microvessels, and may be involved in regulating blood-brain barrier (BBB) permeability. To assess the possible role of PDE4D in stroke-related injury in young versus aged rats, we measured microvascular PDE4D expression, parenchymal albumin immunoreactivity, and changes in the inside bore of the brain microvasculature. Ischemia caused severe hippocampal CA1 damage, associated with significant increases in vascular PDE4D and parenchymal albumin immunoreactivities. This effect was greater in the younger animals, which also had a greater increase in PDE4D expression. Ischemia significantly decreased tissue density in the perimicrovascular space in both young and aged animals. In addition, internal bore circumference and cross-sectional area of the hippocampal microvessels increased dramatically following ischemia. Increased PDE4D expression following cerebral ischemia may play a role in changing BBB permeability, which could secondarily affect ischemic outcome.