Скачать презентацию Noninvasive brain stimulation in neurorehabilitation Disclosures Roy Hamilton Скачать презентацию Noninvasive brain stimulation in neurorehabilitation Disclosures Roy Hamilton

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Noninvasive brain stimulation in neurorehabilitation Disclosures Roy Hamilton, MD, MS • Medical consultant for Noninvasive brain stimulation in neurorehabilitation Disclosures Roy Hamilton, MD, MS • Medical consultant for Neuronix, Assistant Professor of Neurology & LTD, Israel Physical Medicine & Rehabilitation • Funding from NIH/NINDS, Director, Laboratory for Cognition & NIH/NIDCD, RWJF, Neural Stimulation Dana Foundation University of Pennsylvania

NIBS in post-stroke neurorehabilitation Post-Stroke Motor & Cognitive Deficits Visuospatial • Common and debilitating NIBS in post-stroke neurorehabilitation Post-Stroke Motor & Cognitive Deficits Visuospatial • Common and debilitating Neglect • Current therapies: Ineffective (at typical doses) • Recovery depends on network reorganization Aphasia Paresis

How do intact cognitive systems work? Reorganized How do. Systems injured systems differ from How do intact cognitive systems work? Reorganized How do. Systems injured systems differ from normal systems? NIBS in cognitive neurorehabilitation: Normal Systems a model system in translational Cognitive Outcomes Cancognitivereorganization of injured neural systems? we facilitate neuroscience Does it work? * Hypothesis-guided Opinions in Neurobiology, 2014 Poeppel D. , Current Neuromodulation et al. Neurology, 2011 Turkeltaub

Interhemispheric Inhibition Model (-) Excite Inhibit • • Low-frequency r. TMS Cathodal t. DCS Interhemispheric Inhibition Model (-) Excite Inhibit • • Low-frequency r. TMS Cathodal t. DCS • • High-frequency r. TMS Anodal t. DCS “All modelsfrom Hamiltonsome are useful” Adapted are wrong, but et al. , 2011 -George E. P. Box

TMS Studies in Post-stroke Paresis Effect size (All studies): 0. 55; 95% CI (0. TMS Studies in Post-stroke Paresis Effect size (All studies): 0. 55; 95% CI (0. 37 -0. 72) Effect size (Contralesional r. TMS): 0. 69; 95% CI (0. 42 -0. 95) Hsu et al. , Stroke, 2012

Contrastim and NICHE • • Contralesional r. TMS + OT vs sham +OT 20 Contrastim and NICHE • • Contralesional r. TMS + OT vs sham +OT 20 r. TMS/10 Sham 18 sessions/6 weeks 1 week, 1 month, 6 month follow-up • • Harvey et al. , 2014, AHA/ASA International Stroke Conference 80% Clinically meaningful response rate Navigated Inhibitory r. TMS in Contralesional Hemisphere Evaluation (NICHE) • Phase III trial • 2 years • 12 sites

% Change in Naming (Post-Pre r. TMS) r. TMS in Aphasia 50 40 30 % Change in Naming (Post-Pre r. TMS) r. TMS in Aphasia 50 40 30 20 10 0 M 1 -10 -20 Ren et al. , PLOS One, 2014 BA 44 Post Ant BA Sham Inf. BA Sup BA 45 r. TMS 45 45 Garcia et al. , Jo. VE, 2013

t. DCS in Aphasia: Promising But Preliminary Small samples Clinical Heterogeneity -Aphasia type -Chronicity t. DCS in Aphasia: Promising But Preliminary Small samples Clinical Heterogeneity -Aphasia type -Chronicity • • • Variable Parameters Limited Follow-up Promising studies ongoing (e. g. Fridriksson) 25 % Change WAB Aphasia Quotient • • Real t. DCS (n=6) 30 Sham Monti et al. , JNNP, 2013 t. DCS (n=4) 20 15 10 5 0 2 Weeks -5 L 2 Months R -10 Multiple Mechanisms of Aphasia Recovery Adapted from Torres et al. , 2013

Koch et al. , 2012 • • Randomized, double-blind, sham-controlled 10 sessions c. TBS Koch et al. , 2012 • • Randomized, double-blind, sham-controlled 10 sessions c. TBS over 2 weeks Intact left parietal cortex 2 week & 4 week follow-up (post-initiation of therapy) 18 subacute ischemic stroke Behavioral Inattention Test Bifocal TMS to assess frontoparietal excitability PPC-M 1 Excitability Behavioral Inhibition Test

t. DCS Enhances Spatial Processing Egocentric Neglect Allocentric Neglect Medina et al. , 2012 t. DCS Enhances Spatial Processing Egocentric Neglect Allocentric Neglect Medina et al. , 2012

Challenges to NIBS in Rehab • No FDA-approved rehab indications to date • Much Challenges to NIBS in Rehab • No FDA-approved rehab indications to date • Much research at proof-of-concept stage Challenges to clinical development of TMS/t. DCS • Phase I: • Dose-effect relationships • Testing of potentially risky populations • Phase II/III: • Recruitment/eligibility challenges • Heterogeneous patient populations • Multiple sessions & attrition • Phase III: • Control group and blinding issues • Heterogeneity of approaches • Small sample sizes/single sites FDA Clinical Trial Phases: Phase I: Screening for safety Phase II: Smaller, controlled trials of efficacy Phase III: Pivotal larger studies of safety and efficacy* *Two positive phase III trials are required for FDA approval.

Other applications in brain injury • TMS as a prognostic indicator of stroke outcomes Other applications in brain injury • TMS as a prognostic indicator of stroke outcomes – Motor tract patency – Marker of plasticity • TMS pre-surgical mapping of motor function and language • NIBs to treat motor, cognitive, neuropsychological disorders associated with TBI

Faculty Roy Hamilton, MD, MS H. Branch Coslett, MD Sudha Kessler, MD Postdoctoral Fellows Faculty Roy Hamilton, MD, MS H. Branch Coslett, MD Sudha Kessler, MD Postdoctoral Fellows Rachel Wurzman, Ph. D Denise Harvey, Ph. D John Megdaglia, Ph. D Students Perelman School Of Medicine Catherine Norise Harrison Mc. Adams Penn School of Nursing Darina Petrovsky, MSN Undergraduates Jay Gill Jill Sorcher Trevin Glasgow Menvekeh Daramay Follow us on Twitter @Penn. Med. LCNS email: braintms@mail. med. upenn. edu LCNS website: http: //www. med. upenn. edu/lcns Collaborators Priyanka Shah-Basak, Ph. D Peter Turkeltaub, MD, Ph. D (Georgetown) Jared Medina, Ph. D (U. Delaware) Margaret Naeser, Ph. D (Boston University) Alvaro Pascual-Leone, MD, Ph. D (Harvard) Research Staff Olufunsho Faseyitan, MS Daniela Sacchetti, MS Juliann Purcell, MSc Felix Gervits, MA