Neuroreport
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Neuropathic pain is a chronic condition lacking effective management and responding poorly to standard treatment protocols. Motor cortex stimulation has emerged as a new and promising therapeutic tool with outcomes potentially affected by the specific causes and location. In this study we report a series of eight cases in the neurosurgery practice of one of the authors (R. ⋯ Furthermore, we found larger pain relief levels in facial pain conditions with versus without anesthesia dolorosa. These results point to utility of motor cortex stimulation in relieving neuropathic pain, as well as better outcomes for patients with facial pain and anesthesia dolorosa. Future studies should incorporate methods to noninvasively trial those patients who may benefit from surgical implantation to predict the outcomes and maximize their negative predictive value.
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Randomized Controlled Trial
Transcranial direct current stimulation of the prefrontal cortex: a means to modulate fear memories.
Targeting memory processes by noninvasive interventions is a potential gateway to modulate fear memories as shown by animal and human studies in recent years. Modulation of fear memories by noninvasive brain stimulation techniques might be an attractive approach, which, however, has not been examined so far. We investigated the effect of transcranial direct current stimulation (tDCS) applied to the right dorsolateral prefrontal cortex and left supraorbital region on fear memories in humans. ⋯ A day later, fear responses of both groups were compared by monitoring skin conductance. On day 3, during fear response assessment, the tDCS group had a significantly (P<0.05) higher mean skin conductance in comparison with the sham group. These results suggest that tDCS (right prefrontal--anodal, left supraorbital--cathodal) enhanced fear memories, possibly by influencing the prefrontal cortex-amygdala circuit underlying the memory for fear.
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Traumatic brain injury is a leading cause of acquired epilepsy. Initially described in 1989, lateral fluid percussion injury (LFPI) has since become the most extensively used and well-characterized rodent traumatic brain injury and post-traumatic epilepsy model. Universal findings, particularly seizures that reliably develop after an initial latent period, are evident across studies from multiple laboratories. ⋯ We previously demonstrated that the rLFPI procedure resulted in post-traumatic seizures and regional gliosis, but had not examined other histopathologic elements. Now, we show apoptotic cell death confined to the perilesional cortex and chronic pathologic changes such as ipsilesional ventriculomegaly that are seen in the classic model. We conclude that the rLFPI method is a viable alternative to classic LFPI, and--being a one-stage procedure--has the advantage of shorter experiment turnaround and reduced exposure to anesthetics.
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Neural interaction between the eye and hand movement centers must be a critical part of the mechanism underlying eye-hand coordination. One of the previous findings supporting this view is smooth pursuit eye movement-induced suppression of motor-evoked potential (MEP) in the hand muscles. The purpose of this study was to determine which descending volleys contributing to MEP are preferentially modulated by smooth pursuit eye movement. ⋯ Smooth pursuit eye movement facilitated MEP elicited by anterior-posterior (AP) current, but this effect was not seen in MEP elicited by lateromedial or posterior-anterior current. Latency of MEP elicited by AP current was significantly longer than latencies of MEPs elicited by other directions of current, indicating that AP current in the brain predominantly elicited later I-waves. We conclude that smooth pursuit eye movement in the steady-state phase preferentially facilitates MEP predominantly elicited by later I-waves generated by AP current in the brain.
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Acute injury to central nervous system (CNS) triggers neurodegenerative processes that can result in serious damage or complete loss of function. After injury, production of transforming growth factor β1 (TGFβ1) increases and initiates creation of a fibrotic scar that prevents normal growth, plasticity, and recovery of damaged neurons. Administration of TGFβ1 antagonists can prevent its pathological effects. ⋯ LY364947, a blocker of TGFβ1 receptor I, prevented these effects, and IP3 receptor blocker 2-aminoethoxydiphenyl borate (2APB) mimicked them. After CNS injury TGFβ1 downregulates intracellular Ca levels and alters Ca signaling within injured neurons. We suggest that in our model TGFβ1 may trigger both neurodegenerative and neuroprotective events through IP3-induced Ca signaling.