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Multi-Modal Therapy forMulti-Modal Therapy for
Disorders of ConsciousnessDisorders of Consciousness
Philip DeFina, Ph.D.Ph...
Presentation OutlinePresentation Outline
1.1. Need for Improved Therapies for DOCNeed for Improved Therapies for DOC
2.2. ...
1. Need for Improved Therapies1. Need for Improved Therapies
 Traumatic brain injury:Traumatic brain injury:
 33% of adu...
Need for Improved TherapiesNeed for Improved Therapies
 The literature suggests that Severe DisordersThe literature sugge...
Need for Improved TherapiesNeed for Improved Therapies
 These patients are typically medically categorized asThese patien...
Need for Improved TherapiesNeed for Improved Therapies
 In the US, the insurance industry does not
recognize treatment fo...
Need for Improved TherapiesNeed for Improved Therapies
 Specific pharmacological interventions,Specific pharmacological i...
2. Theory of Post-Injury2. Theory of Post-Injury
Reorganization and PlasticityReorganization and Plasticity
 Injured brai...
Diffuse Axonal Injury
 Result of mechanically induced stretching, shearing or
tearing of nerve fibers
 primary pathologi...
Plasticity Following Injury
 Long-Term Potentiation (LTP) is
reduced (Hebb, 1949)
 Long-Term Depression (LTD)
increased;...
NeuromodulationNeuromodulation
By identifying the unique injuryBy identifying the unique injury
characteristics within the...
Complex Intervention vs. SingleComplex Intervention vs. Single
Variable Research ParadigmVariable Research Paradigm
 Trad...
StandardStandard Model for Assessment/Treatment ofModel for Assessment/Treatment of
AcuteAcute Stage TBIStage TBI
 Coma R...
IBRFIBRF Model for Assessment/Treatment ofModel for Assessment/Treatment of
AcuteAcute Stage TBIStage TBI
Directional Norm...
StandardStandard Model for Assessment/Treatment ofModel for Assessment/Treatment of
ChronicChronic Stage TBIStage TBI
 As...
IBRFIBRF Model for Assessment/Treatment ofModel for Assessment/Treatment of
ChronicChronic Stage TBIStage TBI
 Identifica...
IBRF Integrated Multi-modalIBRF Integrated Multi-modal
ApproachApproach
IBRF Program Goals:IBRF Program Goals:
1)1) IdentifyIdentify functional neuromarkersfunctional neuromarkers to establishto...
IBRF Brain Injury ModelIBRF Brain Injury Model
 Assessing Non-Invasive Multimodal FunctionalAssessing Non-Invasive Multim...
IBRFIBRF
Assessment – Treatment – Feedback LoopAssessment – Treatment – Feedback Loop
Clinical
Outcome
Treatment
Intervent...
Integrated Functional Mapping:Integrated Functional Mapping:
The IBRF ApproachThe IBRF Approach
Measure Marker Strengths A...
IBRF-DOC Theoretical ParadigmIBRF-DOC Theoretical Paradigm ––
A Model Based on Neurochemical AutoregulationA Model Based o...
Multi-modal Care ProtocolMulti-modal Care Protocol
(MCP)(MCP)
 Screening:Screening:
 Inclusion/Exclusion CriteriaInclusi...
MCP Retrospective StudyMCP Retrospective Study
 Retrospective Case Series of dataRetrospective Case Series of data
collec...
Participant CharacteristicsParticipant Characteristics
Pre and Post MeasuresPre and Post Measures
 Disability Rating ScaleDisability Rating Scale
 Functional Independence Meas...
DRS, GCS, CRS-R, and Total FIM Scores Between
Admission and Discharge for Entire Sample.
Prognosis for Recovery in DOC Patients Receiving ACP vs.
Standard Care in Published Literature.*
*Clinical change for VS p...
Retrospective ResultsRetrospective Results
 Patients showed statistically significantPatients showed statistically signif...
Sample EEG Data from Retrospective Analysis
Polypharmacy and RiskPolypharmacy and Risk
 Use of multiple medications is routineUse of multiple medications is routine
...
LimitationsLimitations
of Retrospective Studyof Retrospective Study
 Not a controlled, randomized, double-Not a controlle...
5. Future Directions
Department of DefenseDepartment of Defense
Research Grant ProjectResearch Grant Project
Implementatio...
DoD Research GrantDoD Research Grant
General HypothesesGeneral Hypotheses
1.1. By optimizing the electrochemical status of...
Functional Measurement
Instruments
 Functional Independence Measure (FIM)
 Glasgow Coma Scale (GCS)
 Rancho Level of Co...
Neuromarker Measurement
Instruments
 Electroencephalography (EEG)
 Quantitative EEG (qEEG)
 Evoked Potentials (EPs)
 E...
ACP Interventions
 Neuropsychiatric Pharmacology: Off-label use of pharmaceuticals will be
employed to stabilize neurotra...
Contact InformationContact Information
Philip A. DeFina, PhDPhilip A. DeFina, PhD
Chief Executive and Scientific OfficerCh...
IBRF ACP TeamIBRF ACP Team
(alphabetically)(alphabetically)
 Philip A. DeFina, PhD, CEO, CSO, IBRFPhilip A. DeFina, PhD, ...
IBIA Multimodal Talk Download the PPT Slideshow
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  • After a traumatic injury, 33% of adults in a PVS for one month recovered consciousness within three months, and 52% recovered within one year. After a non-traumatic injury, 11% percent of adults in a PVS for one month recovered consciousness within three months, and 13% recovered within one year. The Traumatic Coma Data Bank study reported that 6.5% of adults in a VS (6 of 93) recovered consciousness within one to three years after injury. Nine of 110 vegetative patients (8.2%), including both traumatic and non-traumatic etiologies, emerged from a vegetative state at the one year mark, and 10% demonstrated partial recovery at the five year mark. The literature suggests that SDOC patients in the United States, with severe TBI and VS for greater than 12 months, or with severe nonTBI and VS for greater than 3 months, will probably never recover.
  • After a traumatic injury, 33% of adults in a PVS for one month recovered consciousness within three months, and 52% recovered within one year. After a non-traumatic injury, 11% percent of adults in a PVS for one month recovered consciousness within three months, and 13% recovered within one year. The Traumatic Coma Data Bank study reported that 6.5% of adults in a VS (6 of 93) recovered consciousness within one to three years after injury. Nine of 110 vegetative patients (8.2%), including both traumatic and non-traumatic etiologies, emerged from a vegetative state at the one year mark, and 10% demonstrated partial recovery at the five year mark. The literature suggests that SDOC patients in the United States, with severe TBI and VS for greater than 12 months, or with severe nonTBI and VS for greater than 3 months, will probably never recover.
  • Neurons – larger connectivity than usual functional influence territory … connected but not recruited.
    Unmasking – removal of tonic inhibition so region of influence quickly increased.
    Anatomical changes – new axon terminals, new synapses.
  • Transcript of "IBIA Multimodal Talk Download the PPT Slideshow"

    1. 1. Multi-Modal Therapy forMulti-Modal Therapy for Disorders of ConsciousnessDisorders of Consciousness Philip DeFina, Ph.D.Philip DeFina, Ph.D. International Brain Research FoundationInternational Brain Research Foundation Jonathan Fellus, M.D.Jonathan Fellus, M.D. Kessler Institute for RehabilitationKessler Institute for Rehabilitation Eighth World Congress on Brain InjuryEighth World Congress on Brain Injury Washington, D.C.Washington, D.C. March 10-14, 2010March 10-14, 2010
    2. 2. Presentation OutlinePresentation Outline 1.1. Need for Improved Therapies for DOCNeed for Improved Therapies for DOC 2.2. Theory of Brain Reorganization andTheory of Brain Reorganization and PlasticityPlasticity 3.3. Multi-modal Care Protocol (MCP)Multi-modal Care Protocol (MCP) 4.4. Future Directions: DoD Research GrantFuture Directions: DoD Research Grant
    3. 3. 1. Need for Improved Therapies1. Need for Improved Therapies  Traumatic brain injury:Traumatic brain injury:  33% of adults in PVS for one month33% of adults in PVS for one month recovered within three months, and 52%recovered within three months, and 52% recovered within one year. (Multi-Society Taskrecovered within one year. (Multi-Society Task Force,Force, NEJMNEJM))  Non-traumatic brain injury:Non-traumatic brain injury:  11% of adults in PVS for one month11% of adults in PVS for one month recovered within three, and 13% recoveredrecovered within three, and 13% recovered within one year.within one year.
    4. 4. Need for Improved TherapiesNeed for Improved Therapies  The literature suggests that Severe DisordersThe literature suggests that Severe Disorders of Consciousness (SDOC) patients in theof Consciousness (SDOC) patients in the United States, with severe TBI and VS forUnited States, with severe TBI and VS for greater than 12 months, or with severegreater than 12 months, or with severe nonTBI and VS for greater than 3 months, willnonTBI and VS for greater than 3 months, will likely never recover.likely never recover.
    5. 5. Need for Improved TherapiesNeed for Improved Therapies  These patients are typically medically categorized asThese patients are typically medically categorized as untreatable.untreatable.  often placed in long-term care facilities or home careoften placed in long-term care facilities or home care that provides only palliative support and deteriorate orthat provides only palliative support and deteriorate or die due to lack of proactive medical treatment and/ordie due to lack of proactive medical treatment and/or opportunistic infectious processes.opportunistic infectious processes.  Places an immense burden on family, community, andPlaces an immense burden on family, community, and the health care system, as it is estimated that 70% ofthe health care system, as it is estimated that 70% of those who are in a minimally conscious state due tothose who are in a minimally conscious state due to trauma remain at a moderate to extremely severe leveltrauma remain at a moderate to extremely severe level of disability one year post injury (Mohonk Report, 2006).of disability one year post injury (Mohonk Report, 2006).
    6. 6. Need for Improved TherapiesNeed for Improved Therapies  In the US, the insurance industry does not recognize treatment for DOC, as evident in the lack of Diagnosis-Related Groups (DRGs) and Current Procedural Terminology (CPT) codes (AMA, 2009).  Life expectance of 8-10 years (MSTF)
    7. 7. Need for Improved TherapiesNeed for Improved Therapies  Specific pharmacological interventions,Specific pharmacological interventions, particularly single medicationparticularly single medication interventions, have been studied, in aninterventions, have been studied, in an attempt to improve recovery from MCSattempt to improve recovery from MCS and VS.and VS.
    8. 8. 2. Theory of Post-Injury2. Theory of Post-Injury Reorganization and PlasticityReorganization and Plasticity  Injured brain reacts in specificInjured brain reacts in specific and significant ways.and significant ways.  Metabolic cascadesMetabolic cascades  ExcitotoxicityExcitotoxicity  Cell death and Apoptosis.Cell death and Apoptosis.
    9. 9. Diffuse Axonal Injury  Result of mechanically induced stretching, shearing or tearing of nerve fibers  primary pathologic feature of brain injury in all severity levels of concussion (Kushner, 2001).  increase in neuronal permeability, especially to Ca2+ (reduced mitochondrial metabolism, reduced ATP production)  not detectable by MRI, CT. EEG can detect DAI (Thatcher, 1998; Collins, 2007; Pardini ,2007) DAI causes damage to cortical structures ⇓ excitatory inputs to the brainstem reticular cells suppressed due to lack of input (Gaetz, 2004) ⇓ Decreased arousal or LOC
    10. 10. Plasticity Following Injury  Long-Term Potentiation (LTP) is reduced (Hebb, 1949)  Long-Term Depression (LTD) increased; i.e. a reduction in efficacy of neuronal synapses (Stent, 1973)  Membrane excitability reduced  Anatomical changes – axon terminals damaged & synapses reduced
    11. 11. NeuromodulationNeuromodulation By identifying the unique injuryBy identifying the unique injury characteristics within the brain’scharacteristics within the brain’s electrochemical environment, we canelectrochemical environment, we can identify and measureidentify and measure neuromarkersneuromarkers.. SSpecific interventions and treatments arepecific interventions and treatments are then applied in an effort to facilitate andthen applied in an effort to facilitate and guide neural plasticity.guide neural plasticity. Defina, P. et al, (2009). The new neuroscience frontier: PromotingDefina, P. et al, (2009). The new neuroscience frontier: Promoting neuroplasticity and brain repair in traumatic brain injury,neuroplasticity and brain repair in traumatic brain injury, The Clinical NeuropsychologistThe Clinical Neuropsychologist, 23 (8), 1391-1399 ., 23 (8), 1391-1399 .
    12. 12. Complex Intervention vs. SingleComplex Intervention vs. Single Variable Research ParadigmVariable Research Paradigm  Traditional Research: single, controlled variablesTraditional Research: single, controlled variables  Reality of Medical Treatments is Complex.Reality of Medical Treatments is Complex.  Multiple Medications and Interventions.Multiple Medications and Interventions.  Single design: Unrealistic, ungeneralizable.Single design: Unrealistic, ungeneralizable.  Paradigm Shift:Paradigm Shift: Shepperd and others (2009).Shepperd and others (2009).  Must move to conduct and review ComplexMust move to conduct and review Complex Interventions.Interventions.  Use Key Components: Trial data, QualitativeUse Key Components: Trial data, Qualitative data, Theory.data, Theory.
    13. 13. StandardStandard Model for Assessment/Treatment ofModel for Assessment/Treatment of AcuteAcute Stage TBIStage TBI  Coma Rating ScalesComa Rating Scales  CT ScanCT Scan  Neurologic exam (e.g. cranial nerves, pupil reactivity)Neurologic exam (e.g. cranial nerves, pupil reactivity)  Seizure prophylaxisSeizure prophylaxis  Blood pressure controlBlood pressure control  Blood gases - MonitorBlood gases - Monitor  Electrolyte balance – MonitorElectrolyte balance – Monitor  Nutritional statusNutritional status  Regulate fluid intakeRegulate fluid intake “Improved survival rates … THEN … sit and wait” Do not greatly improve or speed recovery Not predictive of outcome
    14. 14. IBRFIBRF Model for Assessment/Treatment ofModel for Assessment/Treatment of AcuteAcute Stage TBIStage TBI Directional Normalization of brain:  Electrochemistry O2 perfusion  Glucose metabolism Improve/Optimize: CNS tissue survival arousal  cognition  motor skills
    15. 15. StandardStandard Model for Assessment/Treatment ofModel for Assessment/Treatment of ChronicChronic Stage TBIStage TBI  Assorted NP test measuresAssorted NP test measures  Rating scalesRating scales  Symptom monitoringSymptom monitoring  StandardStandard MRI, CT, EEG (limited correlation withMRI, CT, EEG (limited correlation with functional recovery)functional recovery)  ““sit and wait”sit and wait”  Poor predictor of outcomesPoor predictor of outcomes  No subtypingNo subtyping  Does not translate to (guide) treatment protocolDoes not translate to (guide) treatment protocol  Administered beyond critical time windowAdministered beyond critical time window
    16. 16. IBRFIBRF Model for Assessment/Treatment ofModel for Assessment/Treatment of ChronicChronic Stage TBIStage TBI  Identification of NeuromarkersIdentification of Neuromarkers  Subtyping of injurySubtyping of injury  Predicting recovery timelinePredicting recovery timeline  Direct relationship between assessment andDirect relationship between assessment and treatment protocolstreatment protocols  Neuromarkers/assessments DRIVE interventionsNeuromarkers/assessments DRIVE interventions  Intensive multi-modal therapeuticIntensive multi-modal therapeutic interventions through full potential functionalinterventions through full potential functional recoveryrecovery
    17. 17. IBRF Integrated Multi-modalIBRF Integrated Multi-modal ApproachApproach
    18. 18. IBRF Program Goals:IBRF Program Goals: 1)1) IdentifyIdentify functional neuromarkersfunctional neuromarkers to establishto establish TBI subtypes.TBI subtypes. 2)2) Comprehensively evaluate theComprehensively evaluate the unique patternsunique patterns associated with individual TBI subtypes.associated with individual TBI subtypes. 3)3) Refine integratedRefine integrated multi-modalmulti-modal assessmentsassessments that directly guidethat directly guide multi-modalmulti-modal treatment.treatment. 4)4) Predict treatment outcomes based on TBIPredict treatment outcomes based on TBI subtypessubtypes..
    19. 19. IBRF Brain Injury ModelIBRF Brain Injury Model  Assessing Non-Invasive Multimodal FunctionalAssessing Non-Invasive Multimodal Functional Neuromarkers creates a dynamic and integratedNeuromarkers creates a dynamic and integrated ““Brain MapBrain Map””  Neuromarkers are used to recognize multianalyteNeuromarkers are used to recognize multianalyte profiles of:profiles of:  altered neurophysiological function (electrical,altered neurophysiological function (electrical, chemical, metabolic).chemical, metabolic).  neuronal & structural integrityneuronal & structural integrity  chemical homeostasischemical homeostasis  TheThe Brain MapBrain Map directly guides treatmentdirectly guides treatment interventions which are correlated to theinterventions which are correlated to the assessment measures.assessment measures.
    20. 20. IBRFIBRF Assessment – Treatment – Feedback LoopAssessment – Treatment – Feedback Loop Clinical Outcome Treatment Intervention Neuro-Biomarkers (Neurologic, Physiologic, Psychologic, Biologic) Multi-Modal Neurofunctional Assessment
    21. 21. Integrated Functional Mapping:Integrated Functional Mapping: The IBRF ApproachThe IBRF Approach Measure Marker Strengths Associated Treatment EEG, qEEG electrophysiology High temporal resolution (ms) Source localization of electrical generators in cortex EEG brain-computer interface (BCI) training Guides tDCS and TMS EP, ERP electrophysiological High temporal resolution (ms) Measure processing speed Measure intactness of sensory pathways EEG BCI training Guides tDCS and TMS MEG Brain electromagnetism High temporal resolution Subcortical structures Guides tDCS and TMS B.I.S. Monitor Level of consciousness Real-time measure of patient level of consciousness Determine patient receptiveness to treatment MRI w/ DTI Structural anomalies Brain volume Brain connectivity Guides medical and surgical interventions Neurosurgery Pharmacotherapy MRI Spectroscopy Brain chemistry / metabolites Provides chemical neuromarkers Pharmacotherapy, nutraceuticals PET-CT Metabolic functions Multiple metabolic neuromarkers Pharmacotherapy, nutraceuticals Near Infra-red Spectroscopy O2 concentrations/uptake Non-invasive O2 exchange method Pharmacotherapy, nutraceuticals Median nerve stim Combined neurologic assessment modalities: limitations of one modality are compensated for by others
    22. 22. IBRF-DOC Theoretical ParadigmIBRF-DOC Theoretical Paradigm –– A Model Based on Neurochemical AutoregulationA Model Based on Neurochemical Autoregulation Down RegulationDown Regulation Agonist NT’sAgonist NT’s ConsciousnessConsciousness MCSMCS PVSPVS Agonist NT’sAgonist NT’s Up RegulationUp Regulation COMACOMA down regulation manifests as reduceddown regulation manifests as reduced perceptual awareness & unresponsivenessperceptual awareness & unresponsiveness This model developed by Dr. Philip A. De Fina ©This model developed by Dr. Philip A. De Fina © Brain’s Inherent Protective Mechanism to Sustain Life Endorphins GABA Increase Inhibitory NT’s Antagonist NT’s Block Receptors
    23. 23. Multi-modal Care ProtocolMulti-modal Care Protocol (MCP)(MCP)  Screening:Screening:  Inclusion/Exclusion CriteriaInclusion/Exclusion Criteria  Diagnostics:Diagnostics:  functional neuroimaging (e.g., qEEG)functional neuroimaging (e.g., qEEG)  neurophysiological signal processingneurophysiological signal processing  measures of chemical metabolitesmeasures of chemical metabolites  Treatment:Treatment:  Off-label PharmacologicalOff-label Pharmacological  Median Nerve StimulationMedian Nerve Stimulation  Nutraceutical ComponentsNutraceutical Components
    24. 24. MCP Retrospective StudyMCP Retrospective Study  Retrospective Case Series of dataRetrospective Case Series of data collected at KIR from 2005-2009 (IRBcollected at KIR from 2005-2009 (IRB approved retrospective).approved retrospective).  N=41; VS-TBI, VS-nonTBI, MCS-TBI,N=41; VS-TBI, VS-nonTBI, MCS-TBI, MCS-nonTBI.MCS-nonTBI.  Twelve week interventionTwelve week intervention  Traditional OT, Speech, PTTraditional OT, Speech, PT  Off-label PharmaceuticalsOff-label Pharmaceuticals  Median Nerve StimulationMedian Nerve Stimulation  NutraceuticalsNutraceuticals
    25. 25. Participant CharacteristicsParticipant Characteristics
    26. 26. Pre and Post MeasuresPre and Post Measures  Disability Rating ScaleDisability Rating Scale  Functional Independence MeasureFunctional Independence Measure  Glasgow Coma ScaleGlasgow Coma Scale  Coma Recovery Scale-RevisedComa Recovery Scale-Revised  Clinical DX (VS, MCS, Emerged); basedClinical DX (VS, MCS, Emerged); based on Mohonk criteriaon Mohonk criteria  EEG/QEEG - (data in analysis stage)EEG/QEEG - (data in analysis stage)
    27. 27. DRS, GCS, CRS-R, and Total FIM Scores Between Admission and Discharge for Entire Sample.
    28. 28. Prognosis for Recovery in DOC Patients Receiving ACP vs. Standard Care in Published Literature.* *Clinical change for VS patients was compared to the MSTF11 study; clinical change for MCS patients was estimated based on published DRS scores ranging from none to moderate disability (see page 43 and Table 4 of Giacino & Kalmar, 1997).
    29. 29. Retrospective ResultsRetrospective Results  Patients showed statistically significantPatients showed statistically significant improvement across all measures.improvement across all measures.  100% clinical improvement in MCS.100% clinical improvement in MCS.  78-86% clinical improvement in VS.78-86% clinical improvement in VS.  Significant differences between MCP andSignificant differences between MCP and published literature, based on multiple outcomepublished literature, based on multiple outcome measures.measures.
    30. 30. Sample EEG Data from Retrospective Analysis
    31. 31. Polypharmacy and RiskPolypharmacy and Risk  Use of multiple medications is routineUse of multiple medications is routine in medical treatment: Psychiatric,in medical treatment: Psychiatric, Stroke, etc.Stroke, etc.  Retrospective Study: No adverseRetrospective Study: No adverse effects.effects.  This patient population has beenThis patient population has been offered little hope, given limited lifeoffered little hope, given limited life expectancy.expectancy.
    32. 32. LimitationsLimitations of Retrospective Studyof Retrospective Study  Not a controlled, randomized, double-Not a controlled, randomized, double- blinded clinical trial.blinded clinical trial.  No separate standard of care controlNo separate standard of care control group.group.  Small sample size.Small sample size.  Treatments used in combination, thereforeTreatments used in combination, therefore efficacy of single or different combinationsefficacy of single or different combinations not observed. Nevertheless…it is thenot observed. Nevertheless…it is the combination that seems to have the mostcombination that seems to have the most impact.impact.
    33. 33. 5. Future Directions Department of DefenseDepartment of Defense Research Grant ProjectResearch Grant Project Implementation of Advanced CareImplementation of Advanced Care Protocol (ACP) Research ProjectProtocol (ACP) Research Project for Patients with Disorders offor Patients with Disorders of ConsciousnessConsciousness
    34. 34. DoD Research GrantDoD Research Grant General HypothesesGeneral Hypotheses 1.1. By optimizing the electrochemical status of the brain with theBy optimizing the electrochemical status of the brain with the IBRF ACP/MCP, patients with DOC will exhibit more positiveIBRF ACP/MCP, patients with DOC will exhibit more positive health outcomes than patients who receive a placebo ACP/MCP.health outcomes than patients who receive a placebo ACP/MCP. 2.2. Recovery from DOC is marked by unique and specific patterns ofRecovery from DOC is marked by unique and specific patterns of electrical and chemical neuromarkers.electrical and chemical neuromarkers. There will be two groups of participants:There will be two groups of participants: Group 1: Participants receive 12 weeks of the ACP ProtocolGroup 1: Participants receive 12 weeks of the ACP Protocol Group 2: Participants in a Placebo control group receiving currentGroup 2: Participants in a Placebo control group receiving current medical standard care and placebo ACP Protocol interventions.medical standard care and placebo ACP Protocol interventions.
    35. 35. Functional Measurement Instruments  Functional Independence Measure (FIM)  Glasgow Coma Scale (GCS)  Rancho Level of Cognitive Functioning Scale (LCFS)  Coma Rating Scale-Revised (CRS-R)  Disability Rating Scale (DRS)  Orientation Log (O-Log).
    36. 36. Neuromarker Measurement Instruments  Electroencephalography (EEG)  Quantitative EEG (qEEG)  Evoked Potentials (EPs)  Event Related Potentials (ERP)  Magnetic Resonance Imaging (MRI)  Diffusion Tensor Imaging (DTI)  Susceptibility Weighted Imaging (SWI)  Magnetic Resonance Spectroscopy (MRS)  Autonomic Nervous System monitoring (ANS)  Near Infrared Spectroscopy (NIRS)  Bispectral Index (BIS).
    37. 37. ACP Interventions  Neuropsychiatric Pharmacology: Off-label use of pharmaceuticals will be employed to stabilize neurotransmitter functions.  Nutraceuticals: Nutritive Pharmacology will be used to further brain functions while maintaining effective brain metabolism. A combination of pharmaceutical grade nutrients, vitamins, and antioxidants are used with very specific dosing requirements.  Median Nerve Stimulation (MNS): MNS assists in perfusing oxygen to the brain and increasing blood-brain-barrier permeability. It enhances the effects of medications in regulating neurotransmitter stability cortically and sub-cortically (see Cooper & Cooper)  Occupational, Physical, and Speech Therapies: Administration as is customary in rehabilitation facilities.  Cognitive Enhancement: Cognitive enhancement is a tailored program of individualized interventions that will be applied at the post emergent level. It is the application of a variety of training tasks and methods to help improve brain functions. Such methods may include training in perception, attention, concentration, visual-motor-sensory skills, command following, and use of objects.
    38. 38. Contact InformationContact Information Philip A. DeFina, PhDPhilip A. DeFina, PhD Chief Executive and Scientific OfficerChief Executive and Scientific Officer International Brain Research Foundation, Inc.International Brain Research Foundation, Inc. 100 Menlo Park, Suite 412100 Menlo Park, Suite 412 Edison, NJ 08837Edison, NJ 08837 732-494-7600732-494-7600 732-494-7611 FX732-494-7611 FX pdefina@ibrfinc.orgpdefina@ibrfinc.org www.ibrfinc.orgwww.ibrfinc.org
    39. 39. IBRF ACP TeamIBRF ACP Team (alphabetically)(alphabetically)  Philip A. DeFina, PhD, CEO, CSO, IBRFPhilip A. DeFina, PhD, CEO, CSO, IBRF  John DeLuca, PhD, VP Research., KFRC; Advisory Board, IBRFJohn DeLuca, PhD, VP Research., KFRC; Advisory Board, IBRF  Monika Eller, OTR, Clinical Manager of Inpatient OT, KIRMonika Eller, OTR, Clinical Manager of Inpatient OT, KIR  Jonathan Fellus, MD, Director BI Services, KIR; Advisory Board, IBRFJonathan Fellus, MD, Director BI Services, KIR; Advisory Board, IBRF  Pasquale G. Frisina, PhD, Res. & Outcomes Director., KIR; AssisstantPasquale G. Frisina, PhD, Res. & Outcomes Director., KIR; Assisstant Professor, Mt. Sinai School of Medicine.Professor, Mt. Sinai School of Medicine.  Rosemarie Scolaro Moser, PhD, Dir. Res. Prog., IBRF; Dir. RSM Psych.Ctr.Rosemarie Scolaro Moser, PhD, Dir. Res. Prog., IBRF; Dir. RSM Psych.Ctr.  Charles J. Prestigiacomo, MD, Assoc. Prof, Neurol. Surgery, UMDNJ; BoardCharles J. Prestigiacomo, MD, Assoc. Prof, Neurol. Surgery, UMDNJ; Board Member, IBRFMember, IBRF  Philip Schatz, PhD, Prof., Saint Joseph’s University; IBRF ConsultantPhilip Schatz, PhD, Prof., Saint Joseph’s University; IBRF Consultant  James W.G. Thompson, PhD, Director of Research-TBI/SDOC, IBRFJames W.G. Thompson, PhD, Director of Research-TBI/SDOC, IBRF
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