Neurosurgery
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Brain Machine Interface (BMI) systems allow patients with neurological injuries to control assistive devices using cortical signals produced during motor imagery (MI). To improve BMI performance, we sought to enhance cortical signals by training subjects in MI techniques that induce activation of mirror neuron networks (MNN). ⋯ Motor imagery training that activates mirror neuron networks enhances cortical signals during MI and during the performance of corresponding movements in healthy subjects. As MI-based signals are used to operate BMIs, our research suggests that MNN-based MI training may improve BMI performance. Additionally, VR-based imagery training may provide a benefit over AO training to induce bilateral activation of MNNs.
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124 Endoscopic Trigeminal Nucleus Caudalis Doral Root Entry Zone Lesioning for Atypical Facial Pain.
While many chronic pain conditions are challenging to treat, atypical facial pain including conditions such as anesthesia dolorosa and trigeminal deafferentation are among the most difficult. Patients experience numbness in facial areas that also have constant severe, burning pain. The condition results from traumatic or surgical deafferentation injuries of the first-order trigeminal nerve. Anesthesia dolorosa occurs in up to 4% of patients who have undergone prior trigeminal procedures. Deafferentation releases second-order neurons along the trigeminal pain pathway to generate spontaneous pain signals, without a nociceptive stimulus. Medications used for neuropathic pain are first-line but often ineffective. ⋯ Endoscopic NC DREZ lesioning is a safe, effective, and minimally invasive approach for reducing neural hyper-excitability in second order neurons in patients with intractable atypical facial pain. Longer-term studies and follow-up are needed for these challenging types of craniofacial pain.
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Cerebral arteries innervated by several systems contribute to the control of cerebral blood flow. Subarachnoid hemorrhage causes acutely developed vasospasm by various mechanical and neurochemical mechanisms, cranial parasympathetic nerve ischemia, and related stellate ganglion overdischarges. Dilatatory sensory fibers of cranial parasympathetic nerves and vasospastic fibers of stellate ganglions have a vasoregulatory effect on the cerebral arteries The aim of this study is to investigate the effect of sympathectomy on vasospasm of the middle cerebral artery. ⋯ Sympathetic blockage may be a useful effect in the prevention of cerebral vasospasm and other complications of SAH.
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To investigate the role of cigarette smoke exposure (CSE) in the regulation of cerebral smooth muscle cell (SMC) phenotypic modulation in a NAPDH (NOX)-dependent manner and its effect on cerebral aneurysm (CA) formation and rupture. ⋯ CSE initiates oxidative stress-induced phenotypic modulation of SMCs leading to CA formation and rupture. These molecular changes implicate oxidative stress in the pathogenesis of CAs and may provide a potential target for future therapeutic strategies.
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Posttraumatic stress disorder (PTSD) is one of the hallmark conditions of soldiers returning from Operations Iraqi Freedom and Enduring Freedom, with as many as 20% of soldiers affected. Approximately 30% of patients do not respond to conventional treatment, resulting in a significant unmet treatment need. Amygdalar activity is increased in fear learning and PTSD, leading our group and others to hypothesize that amygdalar stimulation may attenuate PTSD-related symptoms. Prior studies showed decreased avoidance behavior with right amygdalar stimulation in a foot-shock paradigm. However, the underlying molecular mechanisms remain incompletely understood. Human and animal studies indicate an anxiolytic function for the neurotransmitter Neuropeptide Y (NPY) in PTSD patients and models of PTSD. We hypothesized that amygdalar stimulation would attenuate behavioral effects in the predator scent model of PTSD and that effects would be mediated by NPY. ⋯ Bilateral amygdalae stimulation attenuated anxiety-like behavior in the predator scent model of PTSD, and treatment was correlated with increased amygdalar NPY. Amygdalar stimulation may alleviate PTSD symptoms, and these data provide the first evidence of a possible underlying molecular mechanism.