The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform
Mark S George - One of the best experts on this subject based on the ideXlab platform.
-
noninvasive techniques for probing neurocircuitry and treating illness Vagus Nerve Stimulation vns transcranial magnetic Stimulation tms and transcranial direct current Stimulation tdcs
Neuropsychopharmacology, 2010Co-Authors: Mark S George, Gary AstonjonesAbstract:Although the preceding chapters discuss much of the new knowledge of neurocircuitry of neuropsychiatric diseases, and an invasive approach to treatment, this chapter describes and reviews the noninvasive methods of testing circuit-based theories and treating neuropsychiatric diseases that do not involve implanting electrodes into the brain or on its surface. These techniques are transcranial magnetic Stimulation, Vagus Nerve Stimulation, and transcranial direct current Stimulation. Two of these approaches have FDA approval as therapies.
-
a one year comparison of Vagus Nerve Stimulation with treatment as usual for treatment resistant depression
Biological Psychiatry, 2005Co-Authors: Mark S George, Lauren B Marangell, John A Rush, Harold A Sackeim, Robert H. Howland, Stephen K Brannan, Sonia M Davis, Mitchel A Kling, Francisco A Moreno, Barry R RittbergAbstract:Background Previous reports have described the effects of Vagus Nerve Stimulation plus treatment as usual (VNS+TAU) during open trials of patients with treatment-resistant depression (TRD). To better understand these effects on long-term outcome, we compared 12-month VNS+TAU outcomes with those of a comparable TRD group. Methods Admission criteria were similar for those receiving VNS+TAU ( n = 205) or only TAU ( n = 124). In the primary analysis, repeated-measures linear regression was used to compare the VNS+TAU group (monthly data) with the TAU group (quarterly data) according to scores of the 30-item Inventory of Depressive Symptomatology–Self-Report (IDS-SR 30 ). Results The two groups had similar baseline demographic data, psychiatric and treatment histories, and degrees of treatment resistance, except that more TAU participants had at least 10 prior major depressive episodes, and the VNS+TAU group had more electroconvulsive therapy before study entry. Vagus Nerve Stimulation plus treatment as usual was associated with greater improvement per month in IDS-SR 30 than TAU across 12 months ( p .001). Response rates according to the 24-item Hamilton Rating Scale for Depression (last observation carried forward) at 12 months were 27% for VNS+TAU and 13% for TAU ( p .011). Both groups received similar TAU (drugs and electroconvulsive therapy) during follow-up. Conclusions This comparison of two similar but nonrandomized TRD groups showed that VNS+TAU was associated with a greater antidepressant benefit over 12 months.
-
Vagus Nerve Stimulation vns for major depressive episodes one year outcomes
Biological Psychiatry, 2002Co-Authors: Lauren B Marangell, John A Rush, Mark S George, Harold A Sackeim, Christopher R Johnson, Mustafa M Husain, Ziad Nahas, Sarah H LisanbyAbstract:Abstract Background: Vagus Nerve Stimulation has shown promising results in an open, acute phase pilot study of adults in a treatment-resistant major depressive episode. This open, naturalistic follow-up study was conducted to determine whether the initial promising effects were sustained, and whether changes in function would be observed. Methods: Thirty adult outpatients in a treatment-resistant, nonpsychotic major depressive episode received an additional 9 months of Vagus Nerve Stimulation treatment following exit from the 3-month acute study. Changes in psychotropic medications and Vagus Nerve Stimulation stimulus parameters were allowed during this longer-term follow-up study. A priori definitions were used to define response (≥ 50% reduction in baseline Hamilton Rating Scale for Depression total score) and remission (Hamilton Rating Scale for Depression ≤ 10). Results: The response rate was sustained [40% (12/30) to 46% (13/28); p = .317] and the remission rate significantly increased [17% (5/30) to 29% (8/28); p = .045] with an additional 9 months of long-term Vagus Nerve Stimulation treatment after exit from the acute study (1 year total Vagus Nerve Stimulation treatment). Significant improvements in function between acute study exit and the 1-year follow-up assessment as measured by the Medical Outcomes Study Short Form-36 were observed. Conclusions: Longer-term Vagus Nerve Stimulation treatment was associated with sustained symptomatic benefit and sustained or enhanced functional status in this naturalistic follow-up study.
-
Vagus Nerve Stimulation a new tool for brain research and therapy
Biological Psychiatry, 2000Co-Authors: Mark S George, Lauren B Marangell, John A Rush, Harold A Sackeim, Mustafa M Husain, Ziad Nahas, Sarah H Lisanby, Tal Burt, J Goldman, James C BallengerAbstract:Biological psychiatry has a long history of using somatic therapies to treat neuropsychiatric illnesses and to understand brain function. These methods have included neurosurgery, electroconvulsive therapy, and, most recently, transcranial magnetic Stimulation. Fourteen years ago researchers discovered that intermittent electrical Stimulation of the Vagus Nerve produces inhibition of neural processes, which can alter brain electrical activity and terminate seizures in dogs. Since then, approximately 6000 people worldwide have received Vagus Nerve Stimulation for treatment-resistant epilepsy. We review the neurobiology and anatomy of the Vagus Nerve and provide an overview of the Vagus Nerve Stimulation technique. We also describe the safety and potential utility of Vagus Nerve Stimulation as a neuroscience research tool and as a putative treatment for psychiatric conditions. Vagus Nerve Stimulation appears to be a promising new somatic intervention that may improve our understanding of brain function and has promise in the treatment of neuropsychiatric disorders.
Michael P Kilgard - One of the best experts on this subject based on the ideXlab platform.
-
safety feasibility and efficacy of Vagus Nerve Stimulation paired with upper limb rehabilitation after ischemic stroke
Stroke, 2016Co-Authors: Jesse Dawson, David M Pierce, Anand Dixit, P Teresa T J Kimberley, Michele Robertson, Brent Tarver, Omar Hilmi, John Mclean, Kirsten P Forbes, Michael P KilgardAbstract:Background and Purpose—Recent animal studies demonstrate that Vagus Nerve Stimulation (VNS) paired with movement induces movement-specific plasticity in motor cortex and improves forelimb function ...
-
Vagus Nerve Stimulation during rehabilitative training improves forelimb strength following ischemic stroke
Neurobiology of Disease, 2013Co-Authors: Navid Khodaparast, Seth A Hays, Andrew M Sloan, Daniel R Hulsey, Andrea Ruiz, Maritza Pantoja, Robert L Rennaker, Michael P KilgardAbstract:Upper limb impairment is a common debilitating consequence of ischemic stroke. Physical rehabilitation after stroke enhances neuroplasticity and improves limb function, but does not typically restore normal movement. We have recently developed a novel method that uses Vagus Nerve Stimulation (VNS) paired with forelimb movements to drive specific, long-lasting map plasticity in rat primary motor cortex. Here we report that VNS paired with rehabilitative training can enhance recovery of forelimb force generation following infarction of primary motor cortex in rats. Quantitative measures of forelimb function returned to pre-lesion levels when VNS was delivered during rehab training. Intensive rehab training without VNS failed to restore function back to pre-lesion levels. Animals that received VNS during rehab improved twice as much as rats that received the same rehabilitation without VNS. VNS delivered during physical rehabilitation represents a novel method that may provide long-lasting benefits towards stroke recovery.
Shih-pin Chen - One of the best experts on this subject based on the ideXlab platform.
-
Vagus Nerve Stimulation inhibits cortical spreading depression exclusively through central mechanisms
Pain, 2020Co-Authors: Andreia Morais, Bruce J Simon, David Y. Chung, Rubem Carlos Araújo Guedes, Tao Qin, Tzuting Liu, Homa Sadhegian, Damla Yagmur, Rosangela Mendes Da Silva, Shih-pin ChenAbstract:Experimental and clinical data strongly support Vagus Nerve Stimulation (VNS) as a novel treatment in migraine. Vagus Nerve Stimulation acutely suppresses cortical spreading depression (CSD) susceptibility, an experimental model that has been used to screen for migraine therapies. However, mechanisms underlying VNS efficacy on CSD are unknown. Here, we interrogated the central and peripheral mechanisms using VNS delivered either invasively (iVNS) or noninvasively (nVNS) in male Sprague-Dawley rats. Cortical spreading depression susceptibility was evaluated 40 minutes after the Stimulation. iVNS elevated the electrical CSD threshold more than 2-fold and decreased KCl-induced CSD frequency by 22% when delivered to intact Vagus Nerve. Distal vagotomy did not alter iVNS efficacy (2-fold higher threshold and 19% lower frequency in iVNS vs sham). By contrast, proximal vagotomy completely abolished iVNS effect on CSD. Pharmacological blockade of nucleus tractus solitarius, the main relay for vagal afferents, by lidocaine or glutamate receptor antagonist CNQX also prevented CSD suppression by nVNS. Supporting a role for both norepinephrine and serotonin, CSD suppression by nVNS was inhibited by more than 50% after abrogating norepinephrinergic or serotonergic neurotransmission alone using specific neurotoxins; abrogating both completely blocked the nVNS effect. Our results suggest that VNS inhibits CSD through central afferents relaying in nucleus tractus solitarius and projecting to subcortical neuromodulatory centers providing serotonergic and norepinephrinergic innervation to the cortex.
-
Vagus Nerve Stimulation inhibits cortical spreading depression.
Pain, 2016Co-Authors: Shih-pin Chen, Bruce J Simon, Katharina Eikermann-haerter, De Morais Al, Tao Qin, Zheng Y, Homa Sadeghian, Fumiaki Oka, Cenk AyataAbstract:Vagus Nerve Stimulation has recently been reported to improve symptoms of migraine. Cortical spreading depression is the electrophysiological event underlying migraine aura and is a trigger for headache. We tested whether Vagus Nerve Stimulation inhibits cortical spreading depression to explain its antimigraine effect. Unilateral Vagus Nerve Stimulation was delivered either noninvasively through the skin or directly by electrodes placed around the Nerve. Systemic physiology was monitored throughout the study. Both noninvasive transcutaneous and invasive direct Vagus Nerve Stimulations significantly suppressed spreading depression susceptibility in the occipital cortex in rats. The electrical Stimulation threshold to evoke a spreading depression was elevated by more than 2-fold, the frequency of spreading depressions during continuous topical 1 M KCl was reduced by ∼40%, and propagation speed of spreading depression was reduced by ∼15%. This effect developed within 30 minutes after Vagus Nerve Stimulation and persisted for more than 3 hours. Noninvasive transcutaneous Vagus Nerve Stimulation was as efficacious as direct invasive Vagus Nerve Stimulation, and the efficacy did not differ between the ipsilateral and contralateral hemispheres. Our findings provide a potential mechanism by which Vagus Nerve Stimulation may be efficacious in migraine and suggest that susceptibility to spreading depression is a suitable platform to optimize its efficacy.
Paul P Tak - One of the best experts on this subject based on the ideXlab platform.
-
Vagus Nerve Stimulation a new bioelectronics approach to treat rheumatoid arthritis
Best Practice & Research: Clinical Rheumatology, 2014Co-Authors: F A Koopman, P R Schuurman, M J Vervoordeldonk, Paul P TakAbstract:There has been a marked improvement in the treatment of rheumatoid arthritis (RA), but most patients do not achieve disease remission. Therefore, there is still a need for new treatments. By screening an adenoviral short hairpin RNA library, we discovered that knockdown of the nicotinic acetylcholine receptor type 7 (α7nAChR) in RA fibroblast-like synoviocytes results in an increased production of mediators of inflammation and degradation. The α7nAChR is intimately involved in the cholinergic anti-inflammatory pathway (CAP). This led us to study the effects of α7nAChR activation in an animal model of RA, and we could show that this resulted in reduced arthritis activity. Accordingly, Stimulation of the CAP by Vagus Nerve Stimulation improved experimental arthritis. Conversely, we found aggravation of arthritis activity after unilateral cervical vagotomy as well as in α7nAChR-knockout mice. Together, these data provided the basis for exploration of Vagus Nerve Stimulation in RA patients as a novel anti-inflammatory approach.
Bruce J Simon - One of the best experts on this subject based on the ideXlab platform.
-
Vagus Nerve Stimulation inhibits cortical spreading depression exclusively through central mechanisms
Pain, 2020Co-Authors: Andreia Morais, Bruce J Simon, David Y. Chung, Rubem Carlos Araújo Guedes, Tao Qin, Tzuting Liu, Homa Sadhegian, Damla Yagmur, Rosangela Mendes Da Silva, Shih-pin ChenAbstract:Experimental and clinical data strongly support Vagus Nerve Stimulation (VNS) as a novel treatment in migraine. Vagus Nerve Stimulation acutely suppresses cortical spreading depression (CSD) susceptibility, an experimental model that has been used to screen for migraine therapies. However, mechanisms underlying VNS efficacy on CSD are unknown. Here, we interrogated the central and peripheral mechanisms using VNS delivered either invasively (iVNS) or noninvasively (nVNS) in male Sprague-Dawley rats. Cortical spreading depression susceptibility was evaluated 40 minutes after the Stimulation. iVNS elevated the electrical CSD threshold more than 2-fold and decreased KCl-induced CSD frequency by 22% when delivered to intact Vagus Nerve. Distal vagotomy did not alter iVNS efficacy (2-fold higher threshold and 19% lower frequency in iVNS vs sham). By contrast, proximal vagotomy completely abolished iVNS effect on CSD. Pharmacological blockade of nucleus tractus solitarius, the main relay for vagal afferents, by lidocaine or glutamate receptor antagonist CNQX also prevented CSD suppression by nVNS. Supporting a role for both norepinephrine and serotonin, CSD suppression by nVNS was inhibited by more than 50% after abrogating norepinephrinergic or serotonergic neurotransmission alone using specific neurotoxins; abrogating both completely blocked the nVNS effect. Our results suggest that VNS inhibits CSD through central afferents relaying in nucleus tractus solitarius and projecting to subcortical neuromodulatory centers providing serotonergic and norepinephrinergic innervation to the cortex.
-
Vagus Nerve Stimulation inhibits cortical spreading depression.
Pain, 2016Co-Authors: Shih-pin Chen, Bruce J Simon, Katharina Eikermann-haerter, De Morais Al, Tao Qin, Zheng Y, Homa Sadeghian, Fumiaki Oka, Cenk AyataAbstract:Vagus Nerve Stimulation has recently been reported to improve symptoms of migraine. Cortical spreading depression is the electrophysiological event underlying migraine aura and is a trigger for headache. We tested whether Vagus Nerve Stimulation inhibits cortical spreading depression to explain its antimigraine effect. Unilateral Vagus Nerve Stimulation was delivered either noninvasively through the skin or directly by electrodes placed around the Nerve. Systemic physiology was monitored throughout the study. Both noninvasive transcutaneous and invasive direct Vagus Nerve Stimulations significantly suppressed spreading depression susceptibility in the occipital cortex in rats. The electrical Stimulation threshold to evoke a spreading depression was elevated by more than 2-fold, the frequency of spreading depressions during continuous topical 1 M KCl was reduced by ∼40%, and propagation speed of spreading depression was reduced by ∼15%. This effect developed within 30 minutes after Vagus Nerve Stimulation and persisted for more than 3 hours. Noninvasive transcutaneous Vagus Nerve Stimulation was as efficacious as direct invasive Vagus Nerve Stimulation, and the efficacy did not differ between the ipsilateral and contralateral hemispheres. Our findings provide a potential mechanism by which Vagus Nerve Stimulation may be efficacious in migraine and suggest that susceptibility to spreading depression is a suitable platform to optimize its efficacy.
-
noninvasive Vagus Nerve Stimulation as treatment for trigeminal allodynia
Pain, 2014Co-Authors: Michael L. Oshinsky, Angela L Murphy, Hugh Hekierski, Marnie Cooper, Bruce J SimonAbstract:Abstract Implanted Vagus Nerve Stimulation (VNS) has been used to treat seizures and depression. In this study, we explored the mechanism of action of noninvasive Vagus Nerve Stimulation (nVNS) for the treatment of trigeminal allodynia. Rats were repeatedly infused with inflammatory mediators directly onto the dura, which led to chronic trigeminal allodynia. Administration of nVNS for 2 minutes decreased periorbital sensitivity in rats with periorbital trigeminal allodynia for up to 3.5 hours after Stimulation. Using microdialysis, we quantified levels of extracellular neurotransmitters in the trigeminal nucleus caudalis (TNC). Allodynic rats showed a 7.7 ± 0.9-fold increase in extracellular glutamate in the TNC after i.p. administration of the chemical headache trigger glyceryl trinitrate (GTN; 0.1 mg/kg). Allodynic rats that received nVNS had only a 2.3 ± 0.4-fold increase in extracellular glutamate after GTN, similar to the response in control naive rats. When nVNS was delayed until 120 minutes after GTN treatment, the high levels of glutamate in the TNC were reversed after nVNS. The nVNS Stimulation parameters used in this study did not produce significant changes in blood pressure or heart rate. These data suggest that nVNS may be used to treat trigeminal allodynia.
