Near Infra Red/ LED and QEEG Neurofeedback Protocol TBI - PowerPoint Presentation

Near Infra Red/ LED and QEEG Neurofeedback Protocol TBI & Post Concussion : Implication of Alzheimer’s and Parkinson’s Increased Risk PI.Marvin Berman PhD Quietmind Foundation & Trent W. Nichols MD, Scientific Advisor Quietmind Fnd and CMO Lumineu

TBI

Blast Effect

Brain Damage Associated with TBI and Post Concussion Syndrome

History of Multiple Sport Concussions and TBI,

Background; Statement of the ProblemImpaired cognition is one of the Post Concussion Syndrome and Traumatic Brain Injury (TBI) symptoms in Military &Former NFL players.

Dementia and traumatic brain injuryOver the past 30 years, research has linked moderate and severe traumatic brain injury to a greater risk of developing Alzheimer's disease or another type of dementia years after the original head injury. One of the key studies showing an increased risk found that older adults with a history of moderate traumatic brain injury had a 2.3 times greater risk of developing Alzheimer's than seniors with no history of head injury, and those with a history of severe traumatic brain injury had a 4.5 times greater risk. Does every hit to the head lead to dementia? Not everyone who experiences a head injury develops dementia. Emerging evidence suggests that individuals who have experienced repeated traumatic brain injuries (concussions) or multiple blows to the head without loss of consciousness, such as professional athletes and combat veterans, are at higher risk of developing a brain condition called chronic traumatic encephalopathy (CTE) than individuals who have not experienced repeated brain injuries. Current research on how traumatic brain injury changes brain chemistry indicates a relationship between traumatic brain injury and hallmark protein abnormalities (beta-amyloid and tau) linked to Alzheimer's. Some research suggests that traumatic brain injury may be more likely to cause dementia in individuals who have a variation of the gene for apolipoprotein E (APOE) called APOE-e4. More research is needed to understand the link between APOE-e4 and dementia risk in those who've had a brain injury.

Closed Head Injury TBI closed

Molecular mechanism of cognitive dysfunction following TBI

Acute Microglial Activation

Molecular mechanisms modulating Aβ and Tau pathology following injury.

Pathophysiological mechanisms of cell death following TBI.

Factors Affecting Cognitive Reserve in TBI

Persistent cognitive dysfunction after traumatic brain injury: A dopamine hypothesis. Bales W1, Wagner AK, Kline AE, Dixon CE.Neurosci Biobehav Rev. 2009

Hyperphosphorylated Tau and Dysfunctional Neurotubule (CTE)

Synaptic Dysfunction in TBI

Solution to TBI/ Post Concussion SyndromeA open label controlled study follows the Margaret Naesar PhD Study at Jamaica Plains Boston VAH which was conducted to test the treatment effectiveness of red and near-infrared (NIR) light in Gulf War Veterans Injury (GWVI) many of whom had TBI!

NIR Light therapyThis LED Light therapy delivered via painless, non-invasive, light-emitting diodes (LED), for improving cognitive symptoms in the areas of Attention, Executive Function, and Memory in GWVI veterans. Their pilot data show that red/NIR LED therapy effectively reduces cognitive problems - e.g., Executive Function (decision-making, multi-tasking, processing speed) and Verbal Memory-- in chronic, traumatic brain injury (TBI; even 7 years post- TBI).

NIR Light in TBI/Post Concussion SyndromeIncreased regional cerebral blood flow (rCBF) may underlie these effects. They provided pilot data showing increased rCBF on functional MRI scans, following a series of transcranial, red/NIR LED treatments of chronic stroke, and of neurodegenerative disease (Primary Progressive Aphasia, similar to Alzheimer’s Disease). Since Chronic Traumatic Encephalopathy (CTE) may occur resulting in progressive dementia i n repeated head trauma and post-concussion syndrome, this intervention with NIR light by Naesar in prior VAH research was found to significantly improved behavior post-therapy .

Mechanism of Action NIR lightThe increase in rCBF (vasodilation) is triggered by release of nitric oxide from hypoxic/compromised cells, after exposure to the red/NIR photons. It has been known since 1981, that approximately 3% of NIR photons applied at the scalp can penetrate 1cm deep, to reach brain cortex

NIR Penetrates the Scalp and Skull

Mechanism of Action NIR Light. In hypoxic/compromised cells, cytochrome C oxidase (the last complex in the electron transport chain) is saturated with nitric oxide; and there is little adenosine tri-phosphate (ATP) production to support needed energy for cellular function. Cytochrome C oxidase is a photo-acceptor for red/NIR wavelengths

PhotoBioModulation on Mitochondria

Mechanism of NIR Light- PhotobiomodulationAfter exposure to the red/NIR photons, the nitric oxide is diffused outside the cell wall where it promotes an increase in vasodilation. At the same time, cytochrome C oxidase increases ATP production in the mitochondria. The cellular effects last beyond the exposure to the red/NIR photons (Lane, 2006). This is referred to as “photobiomodulation

Stimulation of Neurones with NIR Light

ProtocolParticipants;Patients are to be recruited from Quietmind Fnd , SUNY , Wayne State and NFL Wives and possibly local continuing care communities and using print and online media. All subjects will be independently diagnosed with Post- Concussion syndrome, TBI or early CTE by a neurologist by means of the criteria of NIA-OA. [10] Patients will be excluded if there was diagnosis of multi-infarction dementia or Parkinson’s disease under the Quietmind Foundation’s IRB approved randomized, open label controlled design. Informed consent will be obtained prior to initiation of treatment

NIR ProtocolHelmet and Nasal NIR;1. Subjects; 136 or so for 3 year Clinical Study: Subects A group; Randomized to Immediate NBF and B to(12 week delay in Neurobiofeedback) will undergo NIR light therapy after QEEG brain mapping and NIR spectroscopy Frontal and Occipital at baseline, 1 month, 3 months, 6 months and 12 months, 2 and 3 years After subject will undergo QEEG mapping and Neurobiofeedback with either light or music Each subject will be randomized to receive 18 Real red/NIR LED, transcranial treatments; treated 3 xs per week (M, W, and F) for 24 weeks , as an outpatient. Each LED cluster head had a 2-inch diameter, and was 500 mW ; and contained 9 red LED diodes, and 52 NIR LED diodes; power density, 22.2 mW /cm2 . The LED cluster heads were placed bilaterally using the Dougal Helmet (see below) consisting of 18 LED modules. The LED modules cover the forehead and scalp areas including frontal, temporal, parietal and occipital areas, and on the midline (front-to-back hairline) including at the vertex (5 min.) per placement. Home Therapy: Vie Light (gamma) 40Hz Helmet of 4 modules and a nasal infrared light will be used for 20 minutes each treatment day every other day at home following completion of office NIR and NBF . The total treatment visit will lasted about 20 min QOD minutes for 2 1/2 years following Office Dougal Helmet therapy and NBF

Neuro Supplementation ;Dopaplus!Persistent cognitive dysfunction after traumatic brain injury: A dopamine hypothesis . Bales JW1, Wagner AK, Kline AE, Dixon CE. Traumatic brain injury (TBI) represents a significant cause of death and disability in industrialized countries. Of particular importance to patients the chronic effect that TBI has on cognitive function. Therapeutic strategies have been difficult to evaluate because of the complexity of injuries and variety of patient presentations within a TBI population. However, pharmacotherapies targeting dopamine (DA) have consistently shown benefits in attention, behavioral outcome, executive function, and memory. Still it remains unclear what aspect of TBI pathology is targeted by DA therapies and what time-course of treatment is most beneficial for patient outcomes. Fortunately, ongoing research in animal models has begun to elucidate the pathophysiology of DA alterations after TBI. Their review discussing clinical and experimental research examining DAergic therapies after TBI, elucidated the importance of DA for cognitive function/dysfunction after TBI! Hence this-supplementation with DOPA precursors is needed.

Dopaplus® Supplementation 3 capsules contain: folate (as Metafolin ®, L-5-MTHF ) 500 mcg zinc (as zinc picolinate ).10 mg l-tyrosine (free-form) 1,000 mg velvet bean ( mucuna pruriens ) extract (seed ). 200 mg (standardized to contain 15% L-DOPA) rhodiola ( rhodiola rosea ) extract ( root)100 mg (standardized to contain 3% total rosavins and min. 1% salidrosides ) grape ( vitis vinifera ) extract (seed ).100 mg (standardized to contain 92% polyphenols) green tea (camellia sinensis ) extract (leaf ).100 mg (standardized to contain 90% total tea catechins and 70% EGCG) pyridoxal 5’ phosphate (activated B6) 10 mg All subjects will be randomized to receive placebo or active Dopapluse 3 capsules/day for 3 years; Hopefully extension of study for another 7 years by Alzheimer Foundation!

Dougal NIR Helmet

Neuropsychiatric TestingNeuropsychiatric Testing;1.AThe following primary outcome test will be administered: 1) Verbal and Visual Test; Finger Tapping and Symbol Digit Coding test; Stroop (“color-Word” test) (Shifting Attention test), Continuous Performance Test via CNS Vital Signs Computer Report; and 5) Short Form McGill Pain Questionnaire (1984); 6) Overall VAS pain rating ( 0-10 1. Baseline and 2. Week 2 and 4 Group A and B 2. Week 8 and 12 Both Group A and B QEEG mapping and CNS Vital Signs Neurotesting

QEEG & Brain Maping and Neurobiofeedback (NBB)

NIR Spectroscopy

Neural Network Injury Index

Decrease in Chronic Network Z scores also projected after NIR and QEEG NBB

Pre and Post QEEG after Neurobiofeedback

Home therapy with Vielight NIR Helmet and nasal Light