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8/24/2017 1 Tactile Communication & Neuromodulation Laboratory (TCNL) Kinesiology Department, School of Education UW- Madison, Madison, WI, USA 2017, September 14-15, Annual BAAM Fall Conference Traumatic brain injury Leading causes of TBI: Motor-vehicle crashes Falls & sporting accidents Violence & firearms Blasts #1 cause in military Risk factors for TBI: Males 1.5-2 times as likely as females Ages 0-4 years, 15-19, & elderly (>75) African Americans have highest TBI death rate Military duties increase risk of TBI Estimated annual costs from TBI’s: $56.3 billion From www.biausa.org 5.3M living with TBI related disability 1.750 TBI/ year 30% chronic disability 600,000 Retired Soldiers TBI 60,000 Active Duty Soldiers TBI 76.5B Cost to US 30% Chronic Disability Civilian Blunt trauma MVAs, sports, assaults Military US: 2010-2012 - 100,000+ cases 28% of patients at Walter-Reed >$100,000,000/year Explosive blast injury, Overpressure, Penetrating injury, Diffuse axonal injury Army/Civilian Consequences of Concussive Traumatic Brain Injury (TBI) *Worldwide Military TBI Incidence * * Number of cases

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Page 1: 8/24/2017BrainPort Vision Device BrainPort BrainPort Underwater Navigation Device BrainPort Balance Device Electrotactile Brain-Machine Interface Why the tongue? • High density of

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Tactile Communication & Neuromodulation Laboratory (TCNL)Kinesiology Department, School of EducationUW- Madison, Madison, WI, USA

2017, September 14-15,Annual BAAM Fall Conference

Traumatic brain injury

Leading causes of TBI:

•Motor-vehicle crashes

•Falls & sporting accidents

•Violence & firearms

•Blasts #1 cause in military

Risk factors for TBI:

•Males 1.5-2 times as likely asfemales

•Ages 0-4 years, 15-19, &elderly (>75)

•African Americans havehighest TBI death rate

•Military duties increase riskof TBI

Estimated annual costs from TBI’s:

$56.3 billionFrom www.biausa.org

5.3M living with TBI related disability1.750 TBI/ year 30% chronic disability

600,000Retired Soldiers TBI

60,000Active Duty Soldiers TBI

76.5BCost to US

30%Chronic Disability Civilian

Blunt traumaMVAs, sports, assaults

MilitaryUS: 2010-2012 - 100,000+ cases

28% of patients at Walter-Reed>$100,000,000/year

Explosive blast injury,Overpressure,

Penetrating injury,Diffuse axonal injury

Army/Civilian Consequences of Concussive Traumatic Brain Injury (TBI)

*Worldwide Military TBI Incidence

*

*

Number of cases

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From: Mild Traumatic Brain Injury: Neuroimaging of Sports-Related ConcussionJ Neuropsychiatry Clin Neurosci. 2005;17(3):297-303. doi:10.1176/appi.neuropsych.17.3.297

8/24/2017 Biological Processes of Aging, Anatomy 144-575 8

The “bones” of cytoskeleton, form cellular shape“Neurofibrills” - within cytoplasm; responsible for axoplasmic flow (slow),axonal transport (faster),

Neuron: Cytoskeleton

Microtubules = straighthollow pipe, unbranched,~25 nm diameter associated protein –

tubulin (tau); Microtubule-associated

protein, or MAP Neurofilaments =

~ 10 nm have fine branches /like keratin, hair/

Mikrofilaments = associatedprotein actin; ~ 5 nm / like muscle contraction/

8/24/2017 Biological Processes of Aging, Anatomy 144-575 9

Neuron: axonal transport rate

Slow axoplasmictransport rate 0.2-0.4 mm/day ( actin,

tubulin )

Intermediate 15-50 mm/day (mitochondrial

protein)

Fast 200 – 1000 mm/day

(peptides, glyolipids)

No ribosomes in axon !!!Neuritic plaques Neurofilament tangles

TAU protein distribution

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Physical Symptoms

Headache Neck pain Nausea Lack of energy Dizziness Sensitivity to light and sound Ringing in the ears Loss of taste and smell Change in sleep pattern

POST TBI SYMPTOMS

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Cognitive Symptoms

Feeling “dazed” or “foggy” Difficulty concentrating and paying attention Problems with word-finding and putting thoughts into

words Easily confused and loses track of things Slower in thinking, acting, reading, and speaking Easily distracted Trouble doing more than one thing at a time Lack of organization in everyday tasks

POST TBI SYMPTOMS POST TBI SYMPTOMSSocial and Emotional Symptoms

Mood changes including irritability, anxiousness,and tearfulness Decrease motivation Easily overwhelmed More impulsive Withdrawn and wanting to avoid social situations

Personality Changes

Social behavior and Communication skills

Functional SystemApproach

SPLINTERSPLINTER

PAIN

SOLUTION 1SOLUTION 1

SURGERY

MIGRANEMIGRANE

SOLUTION 2SOLUTION 2

PHARMACOLOGY

Parkinson’s Disease

?

...SpeechCognitive disordersMemory lossAttention deficitMovement disordersBalancePostureGaitPTSDDepression...

TBI, Stroke, MS, Alzheimer Disease, Concussions, Brain tumor, …

Solution 1 ?

Solution 3 – Rehabilitation?Solution 2 ?

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PT

OT

DBS

VNS

PaulBach-y-Rita

1934 - 2006

• Sensory Substitution

• Non Synaptic Transmission

• Late Brain Plasticity

TDUTongue Display Unit

Sensory Substitution

BrainPort Vision Device

BrainPortBrainPort UnderwaterNavigation Device

BrainPort Balance Device

ElectrotactileBrain-MachineInterface

Why the tongue?

• High density of sensory nerve endings

• Saliva is excellent electrolyte

• Tongue stays at constant pH+ and tº

• Electrode array is non-invasive

• Discreet protected environment

• Comfortable sensation

• High density of sensory nerve endings

• Saliva is excellent electrolyte

• Tongue stays at constant pH+ and tº

• Electrode array is non-invasive

• Discreet protected environment

• Comfortable sensation

1998

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Relationship of head angleand stimulus position

2-D and 3-D Tongue Threshold Sensitivity Map(N=9)

Vestibular Sensory Substitution System

tcnl.med.wisc.edu

tcnl.med.wisc.edu

Time (sec)

Sway

(deg

.)

0 100 200 300

0 100 200

0 1000 100

0 100 200

0 100 200 300

B

C

A45

0

- 45

45

0

- 45

45

0

- 45

TDU REMOVALBVD Subject CS

SHORT TERM AFTER EFFECT Long Term Residual Effect

100 s

100 s100 s

Subject CS

Ret

entio

n Ef

fect

Time20 min

4-6 h

Long Term Residual Effect Development

0

5

10

7/3/02 9/1/02 10/31/02 12/30/02 2/28/03 4/29/03 6/28/03 8/27/03 10/26/03 12/25/03 2/23/04 4/23/04

Subject CS

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Ret

entio

n Ef

fect

Time20 min

4-6 h

20 min

After 10 training sessions

Scope of Patients Tested

Peripheral

•Ototoxicity•Meniere’s disease•Acoustic Neuroma•Perilymphatic Fistulas•Endolymphatic Hydrops•Vestibular neuritis

•Migraine•Auto Immune degeneration•Mal de Debarquement•Idiopathic origin

•Cerebellar lesion, atrophy•Cerebellar ataxia – stroke•Traumatic Brain Injury•Parkinson’s Disease•MS•Neuropathy

CentralNon-Vestibular

Nature of Deficit Etiologies

Improved Reduced

Common Observations

Balance

Steadiness

Posture

Muscle Tone

Gait

Speech

Sleep

Falls

Depression

Migraine

Rigidity

Fatigue

Oscillopsia

Tinnitus

N=80Late Brain Plasticity

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?????

Sensory Substitution TechnologyBrainPort Devices

CN-NINMCranial NerveNon InvasiveNeuro ModulationTechnology

PoNSPortableNeuroStimulationDevice

2007Information transfer NEUROMODULATION

2010, PoNSTM- 2

NINM Spikes

Synaptic

NeuralNetwork

NonSynaptic Glial

Network

144 electrodes, 1 inch2

50-200 Hz x 20 min5 – 45 000 000

impulses

144 electrodes, 1 inch2

50-200 Hz x 20 min5 – 45 000 000

impulses

tcnl.med.wisc.edu

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DirectNeuronal connections

Indirect connections(interneurons)

Non Synaptictransmission

POST – PRE, few hours after last training

tcnl.med.wisc.edu

Marcus D.A., Furman J.M., Balaban C.D, 2005Motion sickness in migraine sufferersExpert Opin. Pharmacother., 6(15): 2691-2697

EEG recording, Preliminary datain collaboration with Biomedical Engineering DepartmentProfessor Justin Williams; Leo Walton; Adam Wilson

Traumatic brain injury

Results

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TBI - Pilot Study Results gives us confidence

▲=13.5 ▲=14 ▲=10 ▲=21.5

▲=3.0ClinicallySignificantChange

Four female subjects, mean 48.3 y/0Moderate, close-head non-penetrating, concussive TBI9-11 Glasgow Coma ScaleDynamic Gait Index

0

5

10

15

20

25

30

Subject A Subject B Subject C Subject D

GAITDynamic Gait Index (DGI) before and after 5 days of CN-NINM

Before After

DG

I Poi

nts

TBI - Pilot study results gives us confidence

0

10

20

30

40

50

60

70

80

90

100

Subject A Subject B Subject C Subject D

BalanceSensory Organization Test (SOT), Before and After 5 days of CN-NINMTraining

Before After

62

10

22

47

Four female subjects, mean 48.3 y/0Moderate, close-head non-penetrating, concussive TBI9-11 Glasgow Coma ScaleSENSORY ORGANIZATION TEST (SOT)

▲=5.0ClinicallySignificantChange

SOT

Poin

ts

VL – vastus lateralis SOL - Soleus

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SUBJECT MD, 22 yo

00

-10

-20

10

20

SUBJECT AS , 67 yo, APRIL 2012

GAZE, Normal subjects

SUBJECT CA, 16 yo, Sport Concussion,

00 10 20-10-20

SUBJECT AE, 16 yo, Sport Concussion,

00

-10

-20

10

20

SUBJECT AC, 16 yo, Sport Concussion,

00

-10

-20

10

20

SUBJECT AE, 16 yo, Sport Concussion,

00 10 20-10-20

STROKE subject, 80 yo, 7 years after CVA

BEFORE and AFTER 4 month of CN-NINM therapy

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Random Saccade Test, VNG, Stroke, 82 yo Random Saccade Test, VNG, Stroke, 82 yo

Activity Dependent Plasticity

USE IT

LOOSE IT

SPRAUTING

PRUNING

Dendritic arbor Axonal tree

1-1000 spikes/sec

Cell body

Axonal hill

Proximal dendrites

Distal dendrites

Motor

Sensory

• Decreased sensory and motor activity, less spikes• Desynchronization• Less feedback and lateral inhibition• Decreased metabolic rate• Axonal “Pruning”

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• Spike “injection”• Increase metabolic rate• Synaptic plasticity• “Sprouting”

+ Motor

+ Sensory

Disease

CN-NINM

CN-NINM

CN-NINM = Enforced Physical TherapyBrain Stimulation + Exercises (physical, cognitive)

CN-NINM = Rehabilitation Therapy ToolboxPoNS, Face Stimulator, etc. + Training Protocol

CN-NINM is a Symptom Oriented, Multi targeted TherapyMind-Body Interaction, holistic approach

CN-NINM is a patient oriented therapy

CN-NINM is a non invasive and safe therapy

Thank you very much!