Posts Tagged VNS

[Abstract + References] Improving Stroke Rehabilitation with Vagus Nerve Stimulation

Abstract

Stroke is a leading cause of neurological damage, with an estimated 795,000 cases reported in the United States each year. A large percentage of patients who suffer a stroke exhibit long-term impairments in motor function. Poststroke rehabilitation in part aims to promote adaptive changes in neural circuits to support recovery of function, but insufficient or maladaptive plasticity often limits benefits. Adjunctive strategies that support plasticity in conjunction with rehabilitation represent a potential means to improve recovery after stroke. Vagus nerve stimulation (VNS) has emerged as one such targeted plasticity strategy, providing phasic activation of neuromodulatory nuclei associated with plasticity. Repeatedly pairing brief bursts of VNS with motor training drives robust, specific plasticity in neural circuits. A number of studies in animal models of stroke and neurological injury demonstrate that VNS paired with rehabilitative training improves recovery of motor function. Moreover, emerging evidence from clinical trials indicates that VNS delivered during rehabilitation promotes functional recovery in stroke patients. Here, we provide a discussion of the existing literature of VNS-based targeted plasticity therapies in the context of stroke and outline challenges for clinical implementation.

References

  1. 1.
    Benjamin EJ, Blaha MJ, Chiuve SE, Cushman M, Das SR, Deo R, de Ferranti SD, Floyd J, Fornage M, Gillespie C, Isasi CR, Jimenez MC, Jordan LC, Judd SE, Lackland D, Lichtman JH, Lisabeth L, Liu S, Longenecker CT, Mackey RH, Matsushita K, Mozaffarian D, Mussolino ME, Nasir K, Neumar RW, Palaniappan L, Pandey DK, Thiagarajan RR, Reeves MJ, Ritchey M, Rodriguez CJ, Roth GA, Rosamond WD, Sasson C, Towfighi A, Tsao CW, Turner MB, Virani SS, Voeks JH, Willey JZ, Wilkins JT, Wu JH, Alger HM, Wong SS, Muntner P, American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Heart disease and stroke statistics-2017 update: a report from the American Heart Association. Circulation. 2017;135:e146–603.CrossRefPubMedPubMedCentralGoogle Scholar
  2. 2.
    Dobkin BH. Strategies for stroke rehabilitation. Lancet Neurol. 2004;3:528–36.CrossRefPubMedPubMedCentralGoogle Scholar
  3. 3.
    Dobkin BH. Rehabilitation after stroke. N Engl J Med. 2005;352:1677–84.CrossRefPubMedPubMedCentralGoogle Scholar
  4. 4.
    Lai S, Studenski S, Duncan PW, Perera S. Persisting consequences of stroke measured by the stroke impact scale. Stroke. 2002;33:1840–4.CrossRefPubMedGoogle Scholar
  5. 5.
    Calautti C, Baron J. Functional neuroimaging studies of motor recovery after stroke in adults a review. Stroke. 2003;34:1553–66.CrossRefPubMedGoogle Scholar
  6. 6.
    Nudo R, Friel K. Cortical plasticity after stroke: implications for rehabilitation. Rev Neurol. 1999;155:713.PubMedGoogle Scholar
  7. 7.
    Zhang J, Meng L, Qin W, Liu N, Shi FD, Yu C. Structural damage and functional reorganization in ipsilesional m1 in well-recovered patients with subcortical stroke. Stroke. 2014;45:788–93.CrossRefPubMedGoogle Scholar
  8. 8.
    Liepert J, Miltner W, Bauder H, Sommer M, Dettmers C, Taub E, Weiller C. Motor cortex plasticity during constraint-induced movement therapy in stroke patients. Neurosci Lett. 1998;250:5–8.CrossRefPubMedGoogle Scholar
  9. 9.
    Hallett M. Plasticity of the human motor cortex and recovery from stroke. Brain Res Rev. 2001;36:169–74.CrossRefPubMedGoogle Scholar
  10. 10.
    Englot DJ, Rolston JD, Wright CW, Hassnain KH, Chang EF. Rates and predictors of seizure freedom with vagus nerve stimulation for intractable epilepsy. Neurosurgery. 2016;79:345–53.CrossRefPubMedGoogle Scholar
  11. 11.
    Heck C, Helmers SL, DeGiorgio CM. Vagus nerve stimulation therapy, epilepsy, and device parameters scientific basis and recommendations for use. Neurology. 2002;59:S31–7.CrossRefPubMedGoogle Scholar
  12. 12.
    Hays SA. Enhancing rehabilitative therapies with vagus nerve stimulation. Neurotherapeutics. 2016;13(2):382–94.CrossRefPubMedGoogle Scholar
  13. 13.
    Hulsey DR, Riley JR, Loerwald KW, Rennaker RL, Kilgard MP, Hays SA. Parametric characterization of neural activity in the locus coeruleus in response to vagus nerve stimulation. Exp Neurol. 2016;Google Scholar
  14. 14.
    Hulsey DR, Hays SA, Khodaparast N, Ruiz A, Das P, Rennaker RL, Kilgard MP. Reorganization of motor cortex by vagus nerve stimulation requires cholinergic innervation. Brain Stimul. 2016;9(2):174–81.CrossRefPubMedPubMedCentralGoogle Scholar
  15. 15.
    Nichols J, Nichols A, Smirnakis S, Engineer N, Kilgard M, Atzori M. Vagus nerve stimulation modulates cortical synchrony and excitability through the activation of muscarinic receptors. Neuroscience. 2011;189:207–14.CrossRefPubMedGoogle Scholar
  16. 16.
    Seol GH, Ziburkus J, Huang SY, Song L, Kim IT, Takamiya K, Huganir RL, Lee HK, Kirkwood A. Neuromodulators control the polarity of spike-timing-dependent synaptic plasticity. Neuron. 2007;55:919–29.CrossRefPubMedPubMedCentralGoogle Scholar
  17. 17.
    He K, Huertas M, Hong S, Tie X, Hell J, Shouval H, Kirkwood A. Distinct eligibility traces for LTP and LTD in cortical synapses. Neuron. 2015;88:528–38.CrossRefPubMedPubMedCentralGoogle Scholar
  18. 18.
    Flood JF, Smith GE, Morley JE. Modulation of memory processing by cholecystokinin: dependence on the vagus nerve. Science. 1987;236:832–4.CrossRefPubMedGoogle Scholar
  19. 19.
    Flood JF, Morley JE. Effects of bombesin and gastrin-releasing peptide on memory processing. Brain Res. 1988;460:314–22.CrossRefPubMedGoogle Scholar
  20. 20.
    Williams C, Jensen RA. Effects of vagotomy on Leu-enkephalin-induced changes in memory storage processes. Physiol Behav. 1993;54:659–63.CrossRefPubMedGoogle Scholar
  21. 21.
    Jensen RA. Modulation of memory storage processes by peripherally acting pharmacological agents. Proc West Pharmacol Soc. 1996;39:85–9.PubMedGoogle Scholar
  22. 22.
    Talley CP, Clayborn H, Jewel E, McCarty R, Gold PE. Vagotomy attenuates effects of L-glucose but not of D-glucose on spontaneous alternation performance. Physiol Behav. 2002;77:243–9.CrossRefPubMedGoogle Scholar
  23. 23.
    Nogueira PJ, Tomaz C, Williams CL. Contribution of the vagus nerve in mediating the memory-facilitating effects of substance P. Behav Brain Res. 1994;62:165–9.CrossRefPubMedGoogle Scholar
  24. 24.
    Clark K, Krahl S, Smith D, Jensen R. Post-training unilateral vagal stimulation enhances retention performance in the rat. Neurobiol Learn Mem. 1995;63:213–6.CrossRefPubMedGoogle Scholar
  25. 25.
    Clark KB, Naritoku DK, Smith DC, Browning RA, Jensen RA. Enhanced recognition memory following vagus nerve stimulation in human subjects. Nat Neurosci. 1999;2:94–8.CrossRefPubMedGoogle Scholar
  26. 26.
    Engineer ND, Riley JR, Seale JD, Vrana WA, Shetake JA, Sudanagunta SP, Borland MS, Kilgard MP. Reversing pathological neural activity using targeted plasticity. Nature. 2011;470:101–4.CrossRefPubMedPubMedCentralGoogle Scholar
  27. 27.
    Shetake JA, Engineer ND, Vrana WA, Wolf JT, Kilgard MP. Pairing tone trains with vagus nerve stimulation induces temporal plasticity in auditory cortex. Exp Neurol. 2011;233:342–9.CrossRefPubMedGoogle Scholar
  28. 28.
    Engineer CT, Engineer ND, Riley JR, Seale JD, Kilgard MP. Pairing speech sounds with vagus nerve stimulation drives stimulus-specific cortical plasticity. Brain Stimul. 2015;8(3):637–44.CrossRefPubMedPubMedCentralGoogle Scholar
  29. 29.
    Borland MS, Vrana WA, Moreno NA, Fogarty EA, Buell EP, Sharma P, Engineer CT, Kilgard MP. Cortical map plasticity as a function of vagus nerve stimulation intensity. Brain Stimul. 2016;9:117–23.CrossRefPubMedGoogle Scholar
  30. 30.
    Porter BA, Khodaparast N, Fayyaz T, Cheung RJ, Ahmed SS, Vrana WA, Rennaker RL II, Kilgard MP. Repeatedly pairing vagus nerve stimulation with a movement reorganizes primary motor cortex. Cereb Cortex. 2011;22:2365–74.CrossRefPubMedGoogle Scholar
  31. 31.
    Khodaparast N, Hays SA, Sloan AM, Fayyaz T, Hulsey DR, Rennaker RL II, Kilgard MP. Vagus nerve stimulation delivered during motor rehabilitation improves recovery in a rat model of stroke. Neurorehabil Neural Repair. 2014;28:698–706.CrossRefPubMedPubMedCentralGoogle Scholar
  32. 32.
    Hays SA, Khodaparast N, Sloan AM, Fayyaz T, Hulsey DR, Ruiz AD, Pantoja M, Kilgard MP, Rennaker RL II. The bradykinesia assessment task: an automated method to measure forelimb speed in rodents. J Neurosci Methods. 2013;214:52–61.CrossRefPubMedGoogle Scholar
  33. 33.
    Khodaparast N, Hays SA, Sloan AM, Hulsey DR, Ruiz A, Pantoja M, Rennaker RL II, Kilgard MP. Vagus nerve stimulation during rehabilitative training improves forelimb strength following ischemic stroke. Neurobiol Dis. 2013;60:80–8.CrossRefPubMedGoogle Scholar
  34. 34.
    Canning CG, Ada L, Adams R, O’Dwyer NJ. Loss of strength contributes more to physical disability after stroke than loss of dexterity. Clin Rehabil. 2004;18:300–8.CrossRefPubMedGoogle Scholar
  35. 35.
    Harris JE, Eng JJ. Paretic upper-limb strength best explains arm activity in people with stroke. Phys Ther. 2007;87:88–97.CrossRefPubMedGoogle Scholar
  36. 36.
    Hays SA, Khodaparast N, Ruiz A, Sloan AM, Hulsey DR, Rennaker RL, Kilgard MP. The timing and amount of vagus nerve stimulation during rehabilitative training affect post-stroke recovery of forelimb strength. Neuroreport. 2014;25(9):676–82.CrossRefPubMedGoogle Scholar
  37. 37.
    Kelly-Hayes M, Beiser A, Kase CS, Scaramucci A, D’Agostino RB, Wolf PA. The influence of gender and age on disability following ischemic stroke: the Framingham study. J Stroke Cerebrovasc Dis. 2003;12:119–26.CrossRefPubMedGoogle Scholar
  38. 38.
    Freitas C, Perez J, Knobel M, Tormos JM, Oberman L, Eldaief M, Bashir S, Vernet M, Peña-Gómez C, Pascual-Leone A. Changes in cortical plasticity across the lifespan. Front Aging Neurosci. 2011;3Google Scholar
  39. 39.
    Pascual-Leone A, Freitas C, Oberman L, Horvath JC, Halko M, Eldaief M, Bashir S, Vernet M, Shafi M, Westover B. Characterizing brain cortical plasticity and network dynamics across the age-span in health and disease with TMS-EEG and TMS-fMRI. Brain Topogr. 2011;24:302–15.CrossRefPubMedPubMedCentralGoogle Scholar
  40. 40.
    Hays SA, Ruiz A, Bethea T, Khodaparast N, Carmel JB, Rennaker RL, Kilgard MP. Vagus nerve stimulation during rehabilitative training enhances recovery of forelimb function after ischemic stroke in aged rats. Neurobiol Aging. 2016;43:111–8.CrossRefPubMedPubMedCentralGoogle Scholar
  41. 41.
    Bagg S, Pombo AP, Hopman W. Effect of age on functional outcomes after stroke rehabilitation. Stroke. 2002;33:179–85.CrossRefPubMedGoogle Scholar
  42. 42.
    Kwakkel G, Kollen BJ, van der Grond J, Prevo AJH. Probability of regaining dexterity in the flaccid upper limb impact of severity of paresis and time since onset in acute stroke. Stroke. 2003;34:2181–6.CrossRefPubMedGoogle Scholar
  43. 43.
    Biernaskie J, Chernenko G, Corbett D. Efficacy of rehabilitative experience declines with time after focal ischemic brain injury. J Neurosci. 2004;24:1245–54.CrossRefPubMedGoogle Scholar
  44. 44.
    Teasell R, Bitensky J, Salter K, Bayona NA. The role of timing and intensity of rehabilitation therapies. Top Stroke Rehabil. 2005;12:46.CrossRefPubMedGoogle Scholar
  45. 45.
    Salter BK, Hartley BM, Foley BN. Impact of early vs delayed admission to rehabilitation on functional outcomes in persons with stroke. J Rehabil Med. 38, 2006;Google Scholar
  46. 46.
    Khodaparast N, Kilgard MP, Casavant R, Ruiz A, Qureshi I, Ganzer PD, Rennaker RL 2nd, Hays SA. Vagus nerve stimulation during rehabilitative training improves forelimb recovery after chronic ischemic stroke in rats. Neurorehabil Neural Repair. 2016;30(7):676–84.CrossRefPubMedGoogle Scholar
  47. 47.
    Qureshi AI, Tuhrim S, Broderick JP, Batjer HH, Hondo H, Hanley DF. Spontaneous intracerebral hemorrhage. N Engl J Med. 2001;344:1450–60.CrossRefPubMedGoogle Scholar
  48. 48.
    Xi G, Keep RF, Hoff JT. Mechanisms of brain injury after intracerebral haemorrhage. Lancet Neurol. 2006;5:53–63.CrossRefPubMedGoogle Scholar
  49. 49.
    Krishnamurthi RV, Feigin VL, Forouzanfar MH, Mensah GA, Connor M, Bennett DA, Moran AE, Sacco RL, Anderson LM, Truelsen T. Global and regional burden of first-ever ischaemic and haemorrhagic stroke during 1990–2010: findings from the global burden of disease study 2010. Lancet Glob Health. 2013;1:e259–81.CrossRefPubMedPubMedCentralGoogle Scholar
  50. 50.
    Auriat AM, Wowk S, Colbourne F. Rehabilitation after intracerebral hemorrhage in rats improves recovery with enhanced dendritic complexity but no effect on cell proliferation. Behav Brain Res. 2010;214:42–7.CrossRefPubMedGoogle Scholar
  51. 51.
    M. Santos, A. Pagnussat, R. Mestriner, C. Netto. Motor skill training promotes sensorimotor recovery and increases microtubule-associated protein-2 (MAP-2) immunoreactivity in the motor cortex after intracerebral hemorrhage in the rat. ISRN Neurol 2013. (2013).Google Scholar
  52. 52.
    Liang H, Yin Y, Lin T, Guan D, Ma B, Li C, Wang Y, Zhang X. Transplantation of bone marrow stromal cells enhances nerve regeneration of the corticospinal tract and improves recovery of neurological functions in a collagenase-induced rat model of intracerebral hemorrhage. Mol Cells. 2013;36:17–24.CrossRefPubMedPubMedCentralGoogle Scholar
  53. 53.
    Hays SA, Khodaparast N, Hulsey DR, Ruiz A, Sloan AM, Rennaker RL II, Kilgard MP. Vagus nerve stimulation during rehabilitative training improves functional recovery after intracerebral hemorrhage. Stroke. 2014;45(10):3097–30100.CrossRefPubMedPubMedCentralGoogle Scholar
  54. 54.
    Pruitt D, Schmid A, Kim L, Abe C, Trieu J, Choua C, Hays S, Kilgard M, Rennaker RL II. Vagus nerve stimulation delivered with motor training enhances recovery of function after traumatic brain injury. J Neurotrauma. 2016;33(9):871–9.CrossRefPubMedPubMedCentralGoogle Scholar
  55. 55.
    Dawson J, Pierce D, Dixit A, Kimberley TJ, Robertson M, Tarver B, Hilmi O, McLean J, Forbes K, Kilgard MP, Rennaker RL, Cramer SC, Walters M, Engineer N. Safety, feasibility, and efficacy of vagus nerve stimulation paired with upper-limb rehabilitation after ischemic stroke. Stroke. 2016;47:143–50.CrossRefPubMedGoogle Scholar
  56. 56.
    Clinical Trials Identifier: NCT01669161, Paired vagus nerve stimulation (VNS) with rehabilitation for upper limb function improvement after stroke. ClinicalTrials. gov. Bethesda: National Library of Medicine (US). https://clinicaltrials.gov/ct2/show/NCT01669161 (2014).
  57. 57.
    Dawson J, McGrane F. Vagus nerve stimulation and upper limb rehabilitation. Curr Phys Med Rehabil Rep. 2016;4:186–9.CrossRefGoogle Scholar
  58. 58.
    Clinical Trials Identifier: NCT02243020, .VNS during rehabilitation for improved upper limb motor function after stroke. ClinicalTrials. gov. Bethesda: National Library of Medicine (US). https://clinicaltrials.gov/ct2/show/study/NCT02243020 (2014).
  59. 59.
    Krahl SE, Senanayake SS, Handforth A. Destruction of peripheral C-fibers does not Alter subsequent vagus nerve stimulation-induced seizure suppression in rats. Epilepsia. 2001;42:586–9.CrossRefPubMedGoogle Scholar
  60. 60.
    Ruffoli R, Giorgi FS, Pizzanelli C, Murri L, Paparelli A, Fornai F. The chemical neuroanatomy of vagus nerve stimulation. J Chem Neuroanat. 2011;42:288–96.CrossRefPubMedGoogle Scholar
  61. 61.
    Evans M, Verma-Ahuja S, Naritoku D, Espinosa J. Intraoperative human vagus nerve compound action potentials. Acta Neurol Scand. 2004;110:232–8.CrossRefPubMedGoogle Scholar
  62. 62.
    T. Verlinden, K. Rijkers, G. Hoogland, A. Herrler. Morphology of the human cervical vagus nerve: implications for vagus nerve stimulation treatment. Acta Neurol Scand. (2015).Google Scholar
  63. 63.
    Hammer N, Glätzner J, Feja C, Kühne C, Meixensberger J, Planitzer U, Schleifenbaum S, Tillmann BN, Winkler D. Human vagus nerve branching in the cervical region. PLoS One. 2015;10:e0118006.CrossRefPubMedPubMedCentralGoogle Scholar
  64. 64.
    U. Planitzer, N. Hammer, I. Bechmann, J. Glätzner, S. Löffler, R. Möbius, B. N. Tillmann, D. Weise, D. Winkler. Positional relations of the cervical vagus nerve revisited. In: Neuromodulation: technology at the neural interface. (2017).Google Scholar
  65. 65.
    Roosevelt RW, Smith DC, Clough RW, Jensen RA, Browning RA. Increased extracellular concentrations of norepinephrine in cortex and hippocampus following vagus nerve stimulation in the rat. Brain Res. 2006;1119:124–32.CrossRefPubMedPubMedCentralGoogle Scholar
  66. 66.
    Castoro MA, Yoo PB, Hincapie JG, Hamann JJ, Ruble SB, Wolf PD, Grill WM. Excitation properties of the right cervical vagus nerve in adult dogs. Exp Neurol. 2011;227:62–8.CrossRefPubMedGoogle Scholar
  67. 67.
    Mollet L, Raedt R, Delbeke J, El Tahry R, Grimonprez A, Dauwe I, De Herdt V, Meurs A, Wadman W, Boon P. Electrophysiological responses from vagus nerve stimulation in rats. Int J Neural Syst. 2013;23:1350027.CrossRefPubMedGoogle Scholar
  68. 68.
    Clark K, Smith D, Hassert D, Browning R, Naritoku D, Jensen R. Posttraining electrical stimulation of vagal afferents with concomitant vagal efferent inactivation enhances memory storage processes in the rat. Neurobiol Learn Mem. 1998;70:364–73.CrossRefPubMedGoogle Scholar
  69. 69.
    Follesa P, Biggio F, Gorini G, Caria S, Talani G, Dazzi L, Puligheddu M, Marrosu F, Biggio G. Vagus nerve stimulation increases norepinephrine concentration and the gene expression of BDNF and bFGF in the rat brain. Brain Res. 2007;1179:28–34.CrossRefPubMedGoogle Scholar
  70. 70.
    Ploughman M, Windle V, MacLellan CL, White N, Doré JJ, Corbett D. Brain-derived neurotrophic factor contributes to recovery of skilled reaching after focal ischemia in rats. Stroke. 2009;40:1490–5.CrossRefPubMedGoogle Scholar
  71. 71.
    Schäbitz W, Berger C, Kollmar R, Seitz M, Tanay E, Kiessling M, Schwab S, Sommer C. Effect of brain-derived neurotrophic factor treatment and forced arm use on functional motor recovery after small cortical ischemia. Stroke. 2004;35:992–7.CrossRefPubMedGoogle Scholar
  72. 72.
    Dan Y, Poo M. Spike timing-dependent plasticity of neural circuits. Neuron. 2004;44:23–30.CrossRefPubMedGoogle Scholar
  73. 73.
    Alvarez-Dieppa AC, Griffin K, Cavalier S, McIntyre CK. Vagus nerve stimulation enhances extinction of conditioned fear in rats and modulates arc protein, CaMKII, and GluN2B-containing NMDA receptors in the basolateral amygdala. Neural Plast. 2016;2016Google Scholar
  74. 74.
    Xu T, Yu X, Perlik AJ, Tobin WF, Zweig JA, Tennant K, Jones T, Zuo Y. Rapid formation and selective stabilization of synapses for enduring motor memories. Nature. 2009;462:915–9.CrossRefPubMedPubMedCentralGoogle Scholar
  75. 75.
    Ay I, Lu J, Ay H, Gregory Sorensen A. Vagus nerve stimulation reduces infarct size in rat focal cerebral ischemia. Neurosci Lett. 2009;459:147–51.CrossRefPubMedGoogle Scholar
  76. 76.
    Ay I, Ay H. Ablation of the sphenopalatine ganglion does not attenuate the infarct reducing effect of vagus nerve stimulation. Auton Neurosci. 2013;174:31–5.CrossRefPubMedGoogle Scholar
  77. 77.
    Ay I, Nasser R, Simon B, Ay H. Transcutaneous cervical vagus nerve stimulation ameliorates acute ischemic injury in rats. Brain Stimul. 2015;9(2):166–73.CrossRefPubMedPubMedCentralGoogle Scholar

via Improving Stroke Rehabilitation with Vagus Nerve Stimulation | SpringerLink

, , , , ,

Leave a comment

[WEB SITE] Vagus nerve stimulation accelerates motor skill recovery after stroke

Researchers at The University of Texas at Dallas have demonstrated a method to accelerate motor skill recovery after a stroke by helping the brain reorganize itself more quickly.

In a preclinical study, the scientists paired vagus nerve stimulation (VNS) with a physical therapy task aimed at improving the function of an upper limb in rodents. The results showed a doubled long-term recovery rate relative to current therapy methods, not only in the targeted task but also in similar muscle movements that were not specifically rehabbed. Their work was recently published in the journal Stroke.

A clinical trial to test the technique in humans is underway in Dallas and 15 other sites across the country.

Dr. Michael Kilgard, associate director of the Texas Biomedical Device Center (TxBDC) and Margaret Forde Jonsson Professor of Neuroscience in the School of Behavioral and Brain Sciences, led the research team with Dr. Seth Hays, the TxBDC director of preclinical research and assistant professor of bioengineering in the Erik Jonsson School of Engineering and Computer Science, and postdoctoral researcher Eric Meyers PhD’17.

“Our experiment was designed to ask this new question: After a stroke, do you have to rehabilitate every single action?” Kilgard said. “If VNS helps you, is it only helping with the exact motion or function you paired with stimulation? What we found was that it also improves similar motor skills as well, and that those results were sustained months beyond the completion of VNS-paired therapy.”

Kilgard said the results provide an important step toward creating guidelines for standardized usage of VNS for post-stroke therapy.

“This study tells us that if we use this approach on complicated motor skills, those improvements can filter down to improve simpler movements,” he said.

Building Stronger Cell Connections

When a stroke occurs, nerve cells in the brain can die due to lack of blood flow. An arm’s or a leg’s motor skills fail because, though the nerve cells in the limb are fine, there’s no longer a connection between them and the brain. Established rehab methods bypass the brain’s damaged area and enlist other brain cells to handle the lost functions. However, there aren’t many neurons to spare, so the patient has a long-lasting movement deficit.

The vagus nerve controls the parasympathetic nervous system, which oversees elements of many unconscious body functions, including digestion and circulation. Electrical stimulation of the nerve is achieved via an implanted device in the neck. Already used in humans to treat depression and epilepsy, VNS is a well-documented technique for fine-tuning brain function.

The UT Dallas study’s application of VNS strengthens the communication path to the neurons that are taking over for those damaged by stroke. The experiments showed a threefold-to-fivefold increase in engaged neurons when adding VNS to rehab.

“We have long hypothesized that VNS is making new connections in the brain, but nothing was known for sure,” Hays said. “This is the first evidence that we are driving changes in the brain in animals after brain injury. It’s a big step forward in understanding how the therapy works — this reorganization that we predicted would underlie the benefits of VNS.”

In anticipation of the technique’s eventual use in humans, the team is working on an at-home rehab system targeting the upper limbs.

“We’ve designed a tablet app outlining hand and arm tasks for patients to interact with, delivering VNS as needed,” Meyers said. “We can very precisely assess their performance and monitor recovery remotely. This is all doable at home.”

Expanding the Possibilities for Therapy

The researchers are motivated in part by an understanding of the practical limitations of current therapeutic options for patients.

“If you have a stroke, you may have a limited time with a therapist,” Hays said. “So when we create guidelines for a therapist, we now know to advise doing one complex activity as many times as possible, as opposed to a variety of activities. That was an important finding — it was exciting that not only do we improve the task that we trained on, but also relatively similar tasks. You are getting generalization to related things, and you’re getting sustained improvement months down the line.”

For stroke patients, the opportunity to benefit from this technology may not be far off.

“A clinical trial that started here at UTD is now running nationwide, including at UT Southwestern,” Kilgard said. “They are recruiting patients. People in Dallas can enroll now — which is only fitting, because this work developed here, down to publishing this in a journal of the American Heart Association, which is based here in Dallas. This is a homegrown effort.

“The ongoing clinical trial is the last step in getting approved as an established therapy,” Kilgard said. “We’re hopefully within a year of having this be standard practice for chronic stroke.”

 

via Vagus nerve stimulation accelerates motor skill recovery after stroke

, , , , , , , , , , , , , ,

Leave a comment

[ARTICLE] Safety, Feasibility, and Efficacy of Vagus Nerve Stimulation Paired With Upper-Limb Rehabilitation After Ischemic Stroke – Full Text

Abstract

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 after stroke. We conducted a randomized controlled clinical pilot study of VNS paired with rehabilitation on upper-limb function after ischemic stroke.

Methods—Twenty-one participants with ischemic stroke >6 months before and moderate to severe upper-limb impairment were randomized to VNS plus rehabilitation or rehabilitation alone. Rehabilitation consisted of three 2-hour sessions per week for 6 weeks, each involving >400 movement trials. In the VNS group, movements were paired with 0.5-second VNS. The primary objective was to assess safety and feasibility. Secondary end points included change in upper-limb measures (including the Fugl–Meyer Assessment-Upper Extremity).

Results—Nine participants were randomized to VNS plus rehabilitation and 11 to rehabilitation alone. There were no serious adverse device effects. One patient had transient vocal cord palsy and dysphagia after implantation. Five had minor adverse device effects including nausea and taste disturbance on the evening of therapy. In the intention-to-treat analysis, the change in Fugl–Meyer Assessment-Upper Extremity scores was not significantly different (between-group difference, 5.7 points; 95% confidence interval, −0.4 to 11.8). In the per-protocol analysis, there was a significant difference in change in Fugl–Meyer Assessment-Upper Extremity score (between-group difference, 6.5 points; 95% confidence interval, 0.4 to 12.6).

Conclusions—This study suggests that VNS paired with rehabilitation is feasible and has not raised safety concerns. Additional studies of VNS in adults with chronic stroke will now be performed.

Introduction

Arm weakness is common after stroke, and its treatment is recognized as an area of considerable need.1 Approximately 85% of patients with stroke present with arm weakness,2 and 60% of stroke survivors with nonfunctional arms at 1 week do not recover function by 6 months.3Current treatment for arm weakness typically comprises intensive, task-specific, and repetitive rehabilitative interventions or occasionally methods such as constraint-induced movement therapy and electric neurostimulation.4 A recent meta-analysis and large-scale trials show the effects of current treatments for arm weakness to be modest.5,6 Novel and more effective treatments are needed. Improvement in arm function should improve quality of life for stroke survivors, reduce comorbidities associated with loss of independence, and reduce cost to the healthcare system.7

Intensive training has been shown to facilitate a range of neuroplastic brain events.8 It is possible that augmentation of neuroplasticity to promote reorganization of neural networks is required to more fully recover motor function.9 However, no practical and effective method exists to achieve this and even if such changes occur, it is unclear whether they are clinically meaningful or long term. This study is a preliminary investigation of an intervention designed to promote specific neuroplasticity; vagus nerve stimulation (VNS) paired with movement to drive task-specific plasticity in the motor cortex.1012 VNS activates neurons in the basal forebrain and locus coeruleus and results in release of acetylcholine and norepinephrine, respectively, which are known to facilitate reorganization of cortical networks.13 We recently demonstrated in a rat model of ischemic stroke that pairing forelimb rehabilitation with VNS significantly increases recovery of forelimb speed and strength when compared with rehabilitation alone.14,15 Our subsequent studies demonstrated that VNS paired with rehabilitative training also improves recovery in a rat model of intracerebral hemorrhage,16 and that precise timing of VNS with specific motor movements yields optimal recovery.17

We hypothesize that VNS paired with upper-limb rehabilitation therapy will result in greater recovery of arm function than rehabilitation alone in adults with chronic ischemic stroke. We performed the first-in-human evaluation of VNS paired with upper-limb rehabilitation after ischemic stroke. The main objective of the study was to evaluate the safety and feasibility of paired VNS therapy after stroke and to provide clinical data for sample size calculations for larger studies. […]

 

Continue —> Safety, Feasibility, and Efficacy of Vagus Nerve Stimulation Paired With Upper-Limb Rehabilitation After Ischemic Stroke | Stroke

Figure 1. Schematic of vagus nerve stimulation device use in a typical therapy session.

, , , , , , , ,

Leave a comment

[Abstract] The interaction of pulse width and current intensity on the extent of cortical plasticity evoked by vagus nerve stimulation.

Abstract

Background

Repeatedly pairing a tone with a brief burst of vagus nerve stimulation (VNS) results in a reorganization of primary auditory cortex (A1). The plasticity-enhancing and memory-enhancing effects of VNS follow an inverted-U response to stimulation intensity, in which moderate intensity currents yield greater effects than low or high intensity currents. It is not known how other stimulation parameters effect the plasticity-enhancing effects of VNS.

Objective

We sought to investigate the effect of pulse-width and intensity on VNS efficacy. Here, we used the extent of plasticity induced by VNS-tone pairing to assess VNS efficacy.

Methods

Rats were exposed to a 9 kHz tone paired to VNS with varying current intensities and pulse widths. Cortical plasticity was measured as changes in the percent of area of primary auditory cortex responding to a range of sounds in VNS-treated rats relative to naïve rats.

Results

We find that a combination of low current intensity (200 μA) and short pulse duration (100 μs) is insufficient to drive cortical plasticity. Increasing the pulse duration to 500 μs results in a reorganization of receptive fields in A1 auditory cortex. The extent of plasticity engaged under these conditions is less than that driven by conditions previously reported to drive robust plasticity (800 μA with 100 μs wide pulses).

Conclusion

These results suggest that the plasticity-enhancing and memory-enhancing effects of VNS follow an inverted-U response of stimulation current that is influenced by pulse width. Furthermore, shorter pulse widths may offer a clinical advantage when determining optimal stimulation current. These findings may facilitate determination of optimal VNS parameters for clinical application.

via The interaction of pulse width and current intensity on the extent of cortical plasticity evoked by vagus nerve stimulation – Brain Stimulation: Basic, Translational, and Clinical Research in Neuromodulation

, , , , , ,

Leave a comment

[WEB SITE] Rates and Predictors of Seizure Freedom With Vagus Nerve Stimulation for Intractable Epilepsy – NEUROSURGERY Report

Abstract

BACKGROUND: Neuromodulation-based treatments have become increasingly important in epilepsy treatment. Most patients with epilepsy treated with neuromodulation do not achieve complete seizure freedom, and, therefore, previous studies of vagus nerve stimulation (VNS) therapy have focused instead on reduction of seizure frequency as a measure of treatment response.

OBJECTIVE: To elucidate rates and predictors of seizure freedom with VNS.

METHODS: We examined 5554 patients from the VNS therapy Patient Outcome Registry, and also performed a systematic review of the literature including 2869 patients across 78 studies.

RESULTS: Registry data revealed a progressive increase over time in seizure freedom after VNS therapy. Overall, 49% of patients responded to VNS therapy 0 to 4 months after implantation (≥50% reduction seizure frequency), with 5.1% of patients becoming seizure-free, while 63% of patients were responders at 24 to 48 months, with 8.2% achieving seizure freedom. On multivariate analysis, seizure freedom was predicted by age of epilepsy onset >12 years (odds ratio [OR], 1.89; 95% confidence interval [CI], 1.38-2.58), and predominantly generalized seizure type (OR, 1.36; 95% CI, 1.01-1.82), while overall response to VNS was predicted by nonlesional epilepsy (OR, 1.38; 95% CI, 1.06-1.81). Systematic literature review results were consistent with the registry analysis: At 0 to 4 months, 40.0% of patients had responded to VNS, with 2.6% becoming seizure-free, while at last follow-up, 60.1% of individuals were responders, with 8.0% achieving seizure freedom.

CONCLUSION: Response and seizure freedom rates increase over time with VNS therapy, although complete seizure freedom is achieved in a small percentage of patients.

Source: Open Access: Rates and Predictors of Seizure Freedom With Vagus Nerve Stimulation for Intractable Epilepsy | NEUROSURGERY Report

, , , ,

Leave a comment

[ARTICLE] Rates and Predictors of Seizure Freedom With Vagus Nerve Stimulation for Intractable Epilepsy – Full Text

Abstract

BACKGROUND: Neuromodulation-based treatments have become increasingly important in epilepsy treatment. Most patients with epilepsy treated with neuromodulation do not achieve complete seizure freedom, and, therefore, previous studies of vagus nerve stimulation (VNS) therapy have focused instead on reduction of seizure frequency as a measure of treatment response.

OBJECTIVE: To elucidate rates and predictors of seizure freedom with VNS.

METHODS: We examined 5554 patients from the VNS therapy Patient Outcome Registry, and also performed a systematic review of the literature including 2869 patients across 78 studies.

RESULTS: Registry data revealed a progressive increase over time in seizure freedom after VNS therapy. Overall, 49% of patients responded to VNS therapy 0 to 4 months after implantation (≥50% reduction seizure frequency), with 5.1% of patients becoming seizure-free, while 63% of patients were responders at 24 to 48 months, with 8.2% achieving seizure freedom. On multivariate analysis, seizure freedom was predicted by age of epilepsy onset >12 years (odds ratio [OR], 1.89; 95% confidence interval [CI], 1.38-2.58), and predominantly generalized seizure type (OR, 1.36; 95% CI, 1.01-1.82), while overall response to VNS was predicted by nonlesional epilepsy (OR, 1.38; 95% CI, 1.06-1.81). Systematic literature review results were consistent with the registry analysis: At 0 to 4 months, 40.0% of patients had responded to VNS, with 2.6% becoming seizure-free, while at last follow-up, 60.1% of individuals were responders, with 8.0% achieving seizure freedom.

CONCLUSION: Response and seizure freedom rates increase over time with VNS therapy, although complete seizure freedom is achieved in a small percentage of patients.

 

Approximately 1% of the population has epilepsy, and seizures are refractory to antiepileptic drugs (AEDs) in approximately 30% of these individuals.1 Many patients with drug-resistant temporal or extratemporal lobe epilepsy can become seizure-free with surgical resection or ablation, but other patients with epilepsy are not candidates for resection given the presence of primary generalized seizures, nonlocalizable or multifocal seizure onset, or seizure onset from an eloquent brain region.2-5 Treatments based on neuromodulation, such as vagus nerve stimulation (VNS), have, therefore, become an increasingly important part of multimodal epilepsy treatment. VNS therapy was approved by the US Food and Drug Administration in 1997 as an adjunctive therapy for reducing seizures in patients with medically refractory epilepsy, and more than 80 000 patients have received treatment with VNS.6-8 The efficacy of VNS therapy has been evaluated by randomized controlled trials,9,10 retrospective case series,11,12 meta-analysis,13 and registry-based studies.14 These studies show that about 50% to 60% of patients achieve ≥50% reduction in seizure frequency after 2 years of treatment, and response rates increase over time, likely related to neuromodulatory effects with ongoing stimulation.13 Complete seizure freedom, however, is less common with VNS therapy and other neuromodulation treatment modalities.

Given that a minority of patients achieve seizure freedom with VNS, rates and predictors of seizure freedom have not been well studied and remain poorly understood. The vast majority of studies that evaluate VNS therapy focus on rate of response over time (defined as ≥50% reduction in seizures) and predictors of response; there has never been a large-scale evaluation of seizure freedom as a primary end point in patients treated with VNS. However, seizure freedom is the single best predictor of quality of life in patients with epilepsy,15,16 and therefore a better understanding of seizure freedom rates and predictors in patients treated with VNS therapy is critically needed. Importantly, this information may lead to improved patient selection and counseling in the treatment of drug-resistant epilepsy.

Here, we provide the first large-scale study of VNS therapy with a primary goal of defining seizure freedom rates and predictors, and comparing predictors of seizure freedom with those of overall response to treatment. Our study includes univariate and multivariate analyses of registry data including 5554 patients treated with VNS, and also includes a systematic review of the literature including 2869 patients across 78 studies, to help confirm registry-based results.

Continue —> Rates and Predictors of Seizure Freedom With Vagus Nerve Sti… : Neurosurgery

, , , , , ,

Leave a comment

[WEB SITE] Vagus nerve stimulation and upper limb rehabilitation.

The Upper Limb and Stroke

Arm weakness is common after stroke and its treatment is recognised as an area of considerable need.1 Approximately 85% of patients with stroke present with arm weakness2 and 60% of stroke survivors with poorly functioning arms at one week do not recover meaningful function by six months.3 Arm weakness is a major factor contributing to disability following stroke.4Current treatment for arm weakness typically comprises intensive, task-specific and repetitive rehabilitative interventions or occasionally methods such as constraint induced movement therapy and robotic therapy.5 A recent meta-analysis and large-scale trials show the effects of current treatments for arm weakness to be modest.6,7  Improvement in arm function should improve quality of life for stroke survivors, reduce co-morbidities associated with loss of independence, and reduce cost to the health care system.

Neuroplasticity and Recovery

Neuroplasticity is the brain’s ability to form new neural pathways in response to injury or disease. It has been a target for the treatment of many neurological disorders including epilepsy and tinnitus. Recent studies have suggested that augmentation of neuroplasticity is required to more fully recover motor function.9 Novel techniques that drive the growth of new neural pathways related to motor function are needed;  vagus nerve stimulation (VNS) may achieve this.

Vagus Nerve Stimulation

VNS is the delivery of small electrical impulses to the vagus nerve (Figure 1). VNS activates neurons in the basal forebrain and locus coeruleus and results in the release of acetylcholine and norepinephrine. These neurotransmitters are known to facilitate the reorganisation of cortical networks.10 VNS is already used to treat patients with medically refractory epilepsy, with studies showing a reduction in seizure frequency of 50% in 24.5 to 46.6% of patients.11,12,13 In excess of 75,000 patients with refractory epilepsy have been implanted with VNS devices.14  The concept of using VNS to restore normal neuronal activity / drive neuroplasticity is under investigation in other chronic neurological conditions.

In noise induced tinnitus, cochlear trauma can lead to a disorganised auditory cortex resulting in chronic symptoms.15,16,17 The severity of tinnitus is related to the degree of map re-organisation in the auditory cortex.15,16,17  In pre-clinical studies, pairing auditory tones with brief pulses of VNS has been shown to cause re-organisation of auditory cortex maps specific to that tone.18 Further, noise-exposed rats were noted to have a significant reduction in startle response, presumably due to tinnitus, and pairing VNS with multiple tones reversed this effect.18 Thus, VNS paired with a specific stimulus may drive neuroplasticity specifically for that stimulus, thereby restoring auditory cortex architecture and reducing tinnitus. Studies suggest that VNS may help humans with tinnitus.19 Ten patients known to have unilateral or bilateral tinnitus for over a year received four weeks of VNS paired with auditory tone therapy (using MicroTransponder Inc’s Serenity© system). Subjective and objective primary outcome measures were identified in the form of the Tinnitus Handicap Inventory (THI) and the Minimum Masking Level (MML). In patients who had not been taking drugs which could interfere with VNS (muscarinic antagonists, noradrenergic reuptake inhibitors and γ-amino butyric acid agonists), a significant fall in THI of 28.17% was seen following VNS paired with auditory tones.19 Three out of five such patients had a clinically meaningful decrease in THI (44.3% decrease).19 Similar results were seen in the MML test which detects the lowest level of noise required to “drown out” the tinnitus. Results of a recently completed and larger, double blind and randomised study of VNS paired with auditory tones in tinnitus are eagerly awaited. Another study looked at the use of transcutaneous vagus nerve (t-VNS) stimulation in tinnitus. When used in combination with sound therapy t-VNS was found to modulate auditory cortical activation, resulting in reduced tinnitus and tinnitus associated distress.20

Figure 1: © Images copyright of MicroTransponder The stimulation electrodes of the leads are placed on the left vagus nerve in the left carotid sheath, and the lead is then tunnelled subcutaneously to a subcutaneous pocket created in the left pectoral region where it is attached to the pulse generator. A wireless control interface is used to communicate with the VNS device and deliver stimulation during therapy sessions.

Continue —>  Vagus nerve stimulation and upper limb rehabilitation | ACNR | Online Neurology Journal

, , , , , , , , , ,

Leave a comment

[ARTICLE] Vagus nerve stimulation and upper limb rehabilitation – Full Text

The Upper Limb and Stroke

Arm weakness is common after stroke and its treatment is recognised as an area of considerable need.1 Approximately 85% of patients with stroke present with arm weakness2 and 60% of stroke survivors with poorly functioning arms at one week do not recover meaningful function by six months.3 Arm weakness is a major factor contributing to disability following stroke.4Current treatment for arm weakness typically comprises intensive, task-specific and repetitive rehabilitative interventions or occasionally methods such as constraint induced movement therapy and robotic therapy.5 A recent meta-analysis and large-scale trials show the effects of current treatments for arm weakness to be modest.6,7  Improvement in arm function should improve quality of life for stroke survivors, reduce co-morbidities associated with loss of independence, and reduce cost to the health care system.

Neuroplasticity and Recovery

Neuroplasticity is the brain’s ability to form new neural pathways in response to injury or disease. It has been a target for the treatment of many neurological disorders including epilepsy and tinnitus. Recent studies have suggested that augmentation of neuroplasticity is required to more fully recover motor function.9 Novel techniques that drive the growth of new neural pathways related to motor function are needed;  vagus nerve stimulation (VNS) may achieve this.

Continue —> Vagus nerve stimulation and upper limb rehabilitation | ACNR | Online Neurology Journal

Figure 1: © Images copyright of MicroTransponder The stimulation electrodes of the leads are placed on the left vagus nerve in the left carotid sheath, and the lead is then tunnelled subcutaneously to a subcutaneous pocket created in the left pectoral region where it is attached to the pulse generator. A wireless control interface is used to communicate with the VNS device and deliver stimulation during therapy sessions.

 

, , , , , ,

Leave a comment

[ARTICLE] Vagus nerve stimulation delivered with motor training enhances recovery of function after traumatic brain injury

ABSTRACT

Traumatic Brain Injury (TBI) is one of the largest health problems in the United States, and affects nearly two million people every year. The effects of TBI, including weakness and loss of coordination, can be debilitating and last years after the initial injury. Recovery of motor function is often incomplete. We have developed a method using electrical stimulation of the vagus nerve paired with forelimb use by which we have demonstrated enhanced recovery from ischemic and hemorrhagic stroke. Here we have tested the hypothesis that vagus nerve stimulation (VNS) paired with physical rehabilitation could enhance functional recovery after TBI. We trained rats to pull on a handle to receive a food reward. Following training, they received a controlled-cortical impact (CCI) in the forelimb area of motor cortex opposite the trained forelimb, and were then randomized into two treatment groups. One group of animals received vagus nerve stimulation (VNS) paired with rehabilitative therapy, while another group received rehabilitative therapy without VNS. Following CCI, volitional forelimb strength and task success rate in all animals were significantly reduced. VNS paired with rehabilitative therapy over a period of five weeks significantly increased recovery of both forelimb strength and hit rate on the isometric pull task compared to rehabilitative training without VNS. No significant improvement was observed in the Rehab group. Our findings indicate that VNS paired with rehabilitative therapy enhances functional motor recovery after TBI.

via Vagus nerve stimulation delivered with motor training enhances recovery of function after traumatic brain injury | Abstract.

Detect language
Afrikaans
Albanian
Arabic
Armenian
Azerbaijani
Basque
Bengali
Belarusian
Bulgarian
Catalan
Chinese (Simp)
Chinese (Trad)
Croatian
Czech
Danish
Dutch
English
Esperanto
Estonian
Filipino
Finnish
French
Galician
Georgian
German
Greek
Gujarati
Haitian Creole
Hebrew
Hindi
Hungarian
Icelandic
Indonesian
Irish
Italian
Japanese
Kannada
Korean
Lao
Latin
Latvian
Lithuanian
Macedonian
Malay
Maltese
Norwegian
Persian
Polish
Portuguese
Romanian
Russian
Serbian
Slovak
Slovenian
Spanish
Swahili
Swedish
Tamil
Telugu
Thai
Turkish
Ukrainian
Urdu
Vietnamese
Welsh
Yiddish
Afrikaans
Albanian
Arabic
Armenian
Azerbaijani
Basque
Bengali
Belarusian
Bulgarian
Catalan
Chinese (Simp)
Chinese (Trad)
Croatian
Czech
Danish
Dutch
English
Esperanto
Estonian
Filipino
Finnish
French
Galician
Georgian
German
Greek
Gujarati
Haitian Creole
Hebrew
Hindi
Hungarian
Icelandic
Indonesian
Irish
Italian
Japanese
Kannada
Korean
Lao
Latin
Latvian
Lithuanian
Macedonian
Malay
Maltese
Norwegian
Persian
Polish
Portuguese
Romanian
Russian
Serbian
Slovak
Slovenian
Spanish
Swahili
Swedish
Tamil
Telugu
Thai
Turkish
Ukrainian
Urdu
Vietnamese
Welsh
Yiddish
Text-to-speech function is limited to 100 characters

, , , , ,

Leave a comment

[WEB SITE] Bioengineering Professor Recognized for Stroke Recovery Research

March 25, 2015

UT Dallas’ Dr. Seth Hays was honored by the American Heart Association with the Robert G. Siekert New Investigator in Stroke Award recently at the 2015 International Stroke Conference in Nashville, Tenn.

The award, which is presented each year to one outstanding young scientist, encourages new investigators to undertake or continue stroke-related research.

“It is an honor to be recognized by the American Heart Association, an organization with a long tradition of supporting excellent research,” said Hays, an assistant professor of bioengineering in the Erik Jonsson School of Engineering and Computer Science.

Hays’ recent research focuses on developing vagus nerve stimulation (VNS) to improve recovery of motor function after stroke, traumatic brain injury and spinal cord injury, and explaining in detail the mechanisms engaged by VNS to support functional recovery.

VNS is an FDA-approved method for treating various illnesses, such as depression and epilepsy. It involves sending a mild electric pulse through the vagus nerve, which relays information about the state of the body to the brain. Researchers at UT Dallas are studying a novel implementation of VNS to treat neurological disorders.

The association recognized Hays for his paper “Vagus Nerve Stimulation Enhances Neuroplasticity and Forelimb Recovery after Stroke in Aged Rats.” The study, which Hays presented at the conference on Feb. 12, concludes that VNS paired with rehabilitation enhances neuroplasticity — the ability of the brain to change — and functional recovery in post-stroke, aged rats.

“This research project provides additional evidence supporting the ability of VNS to improve recovery after stroke,” he said. “We are now exploring this in greater detail in order to develop this powerful potential therapy.”

Last year, Hays published papers in Stroke, Neuroreport,  Neurorehabilitation & Neural Repair and Brain Research.

Hays received his undergraduate degree in biomedical engineering from The University of Texas at Austin in 2007. In 2012, he completed his PhD in neuroscience at the University of Texas Southwestern Medical Center.

The first postdoctoral research fellow at the UT Dallas Texas Biomedical Device Center, Hays worked under the direction of Dr. Michael Kilgard and Dr. Robert Rennaker.

Rennaker, director of the center and department head of bioengineering, said Hays excelled as a researcher and a colleague during his two years as a fellow, playing a primary role in writing a successful National Institutes of Health research project grant to fund stroke research.

“Dr. Hays is a great example of how UT Dallas will become a top-tier university and develop a pre-eminent bioengineering program,” Rennaker said.

via Bioengineering Professor Recognized for Stroke Recovery Research – News Center – The University of Texas at Dallas.

, ,

Leave a comment

%d bloggers like this: