Neuro feedback to neurology neurologists perspectivesPresentation Transcript
NEURO FEEDBACK TO NEUROLOGY- NEUROLOGIST’S PERSPECTIVESProf. A.V. SRINIVASAN, MD, DM, Ph.D, F.A.A.N, F.I.A.N, EMERITUS PROFESSOR TAMILNADU DR.M.G.R MEDICAL UNIVERSITY CHENNAI PRESIDENT SABA – INDIAN CHAPTER 11th November 2010
Einstein’s Brain 1879-1955
Einstein’s Brain Einstein died in 1955 at age 76. His brain was stored by Dr Thomas Harvey, pathologist, who performed the autopsy. Harvey cut the brain into 240 pieces, which he kept in jars at his house. Harvey moved around the country but he always brought the brain with him. He eventually sent parts out to be studied to various researchers in the 1980s and 1990s. (Reference: Abraham, C., Possessing Genius: The Bizarre Odyssey of Einsteins Brain, New York: St. Martins Press, 2002)
Einstein’s Brain: Smaller Size 1879-1955
Einstein’s Brain: Parietal lobe Parietal lobes are responsible for visual and 3-D representation and mathematical reasoning. E’s inferior parietal lobules are not divided by major cleft • Not seen in 191 controls! • Axons were connected in unusual ways “might have allowed for his brilliance and his ability to put spatial representations into mathematical concepts”
Einstein’s Brain: Hippocampus E’s left hippocampal neurons were larger in 4 of 5 five regions compared to right. • Controls showed minimal and inconsistent asymmetry. • Larger neurons in left hippocampus, DW Zaidel noted, imply that Einsteins left brain may have had stronger nerve cell connections between the hippocampus and neocortex than his right.
Einstein’s Brain: Other Differences Total brain weight of only 1,230 grams (average same-aged male = 1,350 grams). Thickness of area 9 (prefrontal cortex) was thinner than that of 5 controls, but same number of neurons. • Thus density of neurons in AE’s brain greater.
"On the Brain of a Scientist: Albert Einstein” Diamond, Scheibel, & Murphy (1985) Surveyed neurons and glia in left and right area 9 (important in planning) and area 39 (language and integration) • More glial cells per neuron in AE compared to 11 age-matched male controls. • Left area 39 most significant difference Conclusion: AE’s neurons may have had an increased "metabolic need"
Is brain-behavior behavior? If so, it can be conditioned just like other behaviors In 1960s, certain rhythms could be “trained” Led to Neurotherapy and Brain-Computer interfaces (BCI)
Definition of Learning Learning is an adaptive1 permanent change2 in behavior or behavior potential3 that is produced as a result of prior experience4 1 occasionally maladaptive such as depressed mental set, obsessions 2 not due to fatigue, injury 3 includes tendencies to respond that might not have been tested 4 excludes maturation, disease, instinct
Two forms of conditioning Classical conditioning • Hard-wired linkage between stimulus and response (e.g., food and saliva) • Anything acting as signal of food can produce response Operant conditioning • Training linkage between stimulus and response through reinforcement • behavior strengthened if followed by reinforcement • behavior weakened if followed by punishment • Law of Effect (Thorndike) • Rewarded behavior is repeated
Components of conditioning Acquisition • initial stage of learning, during which a response is established and gradually strengthened Effective pairing of reinforcement
Extinction• diminishing a conditioned response• occurs when an response is not followed by a reward
Extinction and spontaneous recovery Acquisition Strong (response + reward) Spontaneous Extinction recovery of (no reward) response Strength of CR Extinction (no reward) Weak Pause Time
Operant Conditioning Spontaneous recovery • reappearance, after a rest period, of an extinguished conditioned response Generalization • tendency for stimuli similar to the conditioned stimulus to evoke similar responses Discrimination • Identify specific stimulus from set of similar stimuli to evoke similar reinforced responses
When you become aware of your ownbrain activity –you can change it also.
Electrical stimulation of brains (ESB) Electrical stimulation of brains of rats - James Olds in 1950s; • Jacobsen and Torkildsen replicated work in humans; • some epileptics stimulated themselves into convulsions
INTRA-CRANIAL SELF- STIMULATION Rodent wireheads • 0.0005 amps whenever rat pushed lever • Up to 10,000 bar-presses an hour recorded • Animals self-stimulate > 24 hrs continuously without rest, and cross electrified grid to gain access to lever • Reward center: Medial forebrain bundle passing through lateral hypothalamus and ventral tegmentum • Other brain centers are aversive, such as periaqueductal grey matter (PAG) • Ventral tegmental area (VTA) neurons manufacture dopamine and they are under continuous inhibition by gamma-aminobutyric acid (GABA) system, an important component of the ”final common pathway" of reward, implicated in addiction, mood, and learning.
Delgado, Primate wireheads, and Circuitry man
Electrical stimulation of brains (intracranial stimulation) Pavlov conditioning experiments • Tone for food, buzzer for shock – • Moved them closer together in time • confounded dog fell asleep Termed “internal inhibition” Animal can close down own systems to avoid stress Neal E Miller trained autonomic functions • Dogs salivate to get food • Rats control heartrate to get water
History of Biofeedback JH Bair, 1901, instrument used to teach ear wiggling In early 20th century, J.H. Schultz in Germany developed a technique called Autogenic Training. Verbal instructions are used to guide a person to a more relaxed and controlled physiological state. • The method flourished, and the results were reported upon by Wolfgang Luthe in 1969 in the United States. Increased awareness in Western world of yogic ability to alter physiology volitionally. E.g., a yogi could survive in a sealed box by voluntarily reducing his metabolic rate significantly, surviving hours with a limited supply of oxygen. Peripheral biofeedback techniques include • GSR, thermal, breathing, cardiac
History of EEG biofeedback 1934, Adrian watched his EEG in front of oscillograph and created alpha at will Alpha biofeedback or deep states • Joe Kamiya at Univ of Chicago, 1958+ Kamiya 1958 • 1st subject - 60 tones and 60 guesses, half right • 2nd trial, 65 % correct • 3rd 85% correct • 4th, after a few mistakes, 400 correct in a row 1968 first congress in Aspen Colorado, called biofeedback “Alpha training” adopted by flower 1978 Science paper culture of late 1960s, and practitioners oversold its claims
History of SMR biofeedback In 1960s Mercury astronauts claimed they saw natives waving at them when the flew over the Pacific.(i.e., they hallucinated) In 1967, Gordon Allies, inventor of amphetamine, was contracted to test toxicity of the Mercury capsule rocket fuel with David Fairchild However Allies tested another MB Sterman chemical compound on himself and shortly died, before contract over. Fairchild asked Sterman to help finish work.
Sterman was studying EEG-behavioral correlates in cats
If EEG behavior is like any other behavior, it could be shaped with operant conditioning Two prominent rhythms in cat EEG – SMR and PRS • Couldn’t train PRS, but could train SMR • More on the PRS later
Cat Wireheads: cortical electrodes, not brain stem or hypothalamic Cats often used in electrophysiology because head size the same regardless of breed, unlike dogs
10 cats trained to produce SMR (sensorimotoractivity over motor strip) for chicken broth & milk
Acquisition resembles normalbehavior under O.C. training
Classic abundance response at extinction
History of SMR biofeedback Then Sterman and Fairchild went on to another study, testing rocket fuel on 50 cats, 10 from Sterman’s previous SMR training study. Inject 100 mg/kg or so of fuel into each cat • After one hour, all usually go into grand mal but not all - 7 delayed, 3 not at all. • seizure thresholds changed in these 10 • Not explainable by placebo (“i shall please” in Latin) as cats didn’t know what to expect, and experimenter blind because effect was entirely unexpected
Sterman et al (1967) showing usual toxicprodrome and resistance to MMH-induced seizures in a subgroup Time Avg 2 hours+ for seizures with EEG trained cats vs. 1 hour for normal cats NASA Rocket fuel
History of SMR biofeedback Replicated findings in monkeys, then moved to humans at colleagues urging. Human epileptics • First case study published in EEG & Clin Neurophysiology • N=4 study, 65% seizure reduction, in Epilepsia 1976 • Then n=8, ABA three-year study, Epilepsia 1978 • Finally, full blown study funded by NIH Sham control, n=24, three years Double yoked n=8, n=8 NF, n=8 log books many went seizure free controls after study received NF Reliable increase in sleep spindle density and decreased awakenings
A major study showed 60% reduction in seizures 12 months after training
Turf war with medicine In 1982 Sterman’s NIH grant for 3 y was funded, but then they demanded double blind after approving the initial design, then they pulled funding saying goals already reached Cost of temporal lobe resection for epilepsy = $200,000 • Money lost if patient undergoes neurotherapy successfully
Review of 19 studies with EEG Biofeedback for Epilepsy* Medical Journal, Jan 2000 82% of studies demonstrated significant seizure reduction Average reduction exceeded 50%. Studies reported reduction in seizure severity. About 5% had complete control for up to one year* Sterman, MB (2000). Basic Concepts and Clinical Findings in the Treatment of Seizure Disorders with EEG Operant Conditioning. Clinical EEG, 31(1), 45-55.
SMR attenuated (compared to cat subdural recordings) but also present at the scalp in humans
Mechanisms of SMR training Enhancing GABA circuitry involved in motor regulation, dampening excitability to sensorimotor excitation
10-20 International System of Electrode Placement
History of Motoric Hyperexcitability 1905: Hyperkinetic syndrome (George Frederic Still, Lancet) • “wanton destructiveness and a deficit in moral behavior” Now known to be due to slowed maturation • only partly related to will power, if at all Lubar (1975) ABA study, n=4 • Cz theta/beta ratio
Patterns of behavior indicative of ADHD Inattentive • Easily distracted • Fails to pay attention to details makes careless mistakes rarely follows directions completely or properly • Forgets things needed to complete tasks (e.g., pencils) Hyperactive • Unable to sit still Leaves seat when sitting expected or instructed • Talks non-stop Impulsive • Unable to suppress impulses inappropriate comments or shouts out answers early • Hits • Often puts oneself in danger, such as dashes into street
Attention Deficit Hyperactivity Disorder ADHD affects 2 million children in USA • 5% of all boys • 2% of all girls ~ 60% will remain symptomatic as adults 1 M children take Rx to control hyperactivity. Genetic component: MZ concordance is 75-91% EEG frontal slowing due to immature frontal lobe in impulsive subtype
Ritalin Controversy Commonly prescribed drug for children • Worries about long-term effects. • No studies on children who have taken Ritalin > 14 months. • Very similar to cocaine in composition and effect
Monastra study – ADHD and biofeedback vs. stimulant therapy 100 ADHD children, ages 6-19, inattentive or combined types 1-year multimodal outpatient program • included Ritalin, parent counseling, academic support 51 with EEG biofeedback RESULTS • Post Tx assessments with and without stimulant therapy. Ritalin produced significant improvement on TOVA and ADDES • Did not sustain when Ritalin removed EEG biofeedback group sustained gains when Ritalin removed.
First Year of specific Neurofeedback Application 1967 SMR conditioning in general 1973 Epilepsy 1975 Peak Performance 1976 ADHD 1977 Addiction 1978 Anxiety disorders 1978 Learning disabilities 1980 Sleep Disorders 1995 Brain Injury 1995 Lymes Disease 1996 CFS 1997 Mood disorders
Neurotherapy -start Revives Hess’ CNS model of 1950s • overaroused • underaroused Added by Othmers • instability Related issue of plasticity • Cajal thought adult brain fixed • finally countered by Peter Eriksson 1998
Most important figure in behavioral neuroscience (i.e., psychology)
Elegant design to counter anyintrinsic (non-contextual) reward
PRS and learning
PRS characteristics Reward-based inhibition of MRF • Mesencephalic Reticular Formation (originally called ARF) – turns off the DC, i.e., volitional aspect of mind PRS does not occur initially • animal must be fully habituated to environment • any novelty or change will disrupt it. • Light must also be on for PRS to emerge, even when “light off” is a signal of food delivery trials. 3-5 s burst indistinguishable from sleep onset or SWS Signal transmission in thalamus (LGN) and cortex is suppressed by PRS (similar to SWS)
Unresponsive during PRS, like sleep
PRS (6-9 Hz in cats, 8-13 Hz in humans)
Alpha burst reflect preparation
Impact human learning
Field of Neuroregulation Clinical aspects • Thalamocortical dysrhythmias Cognition • Time binding • Information processing, recruitment ERD and ERS
NF Practice Therapist and client/game screen Therapist Monitor EEG SensorsFeedback Screen
Game provides client feedback Mazes
The Therapist Screen RawInhibitRewardInhibit
Scoring Charts Provide Periodic Feedback
A normal looking EEG is small in height Small EEG
Reducing excessive (tall) slow brainwaves helps the brain function better Examples of excessive slow brainwaves
Courtesy ofExample of EEG Brain Map Q-Metrx
This man has way too much alpha withhis eyes open. He’s got problems withobsessive thinking – getting “stuck”Slow alpha increased with eyes open. That’s not normal.
PRE/POST ASSESSMENTSMale, age 9. Drawing before Neurofeedback training
Male, age 9.Drawing after 4 months ofNeurofeedbacktraining, 5/2/95
One year follow-up TOVA Follow-up Summary - (n=16) Courtesy of Moshe Perl, Ph.D. Pretreatment 14 Months Post Treatment Followup 120 110 103 105106 100 99 97 92 94Standard Score 92 90 88 84 80 80 74 70 60 50 40 Inattention Response Time Impulsivity Variability
Brain-Computer Interface (BCI) Muscle-independent communication channel Two general approaches: • rhythm generation (neurofeedback approach) • natural correlates (QEEG assessment approach) Greatest obstacles • Humans habituate • Speed is slow, thus motivation must be high Training also slower for patients, generally, than normals • Interference and distraction (a divided attention task) Current formulations requires a patient to pay attention to contents of communication while simultaneously following generative rules of the communication device. • Impaired visual systems • Instability, noise and/or lack of our understanding of human EEG
Speeds are generally characters per minuteImagery 1. think about nothing 2. solve multiplication 3. mentally rotate 4. mentally write a letter to friend 5. visualize numbers being written on board sequentially
BCI Applications Workload shunting Augmented reality (instead of VR) Locked-in syndrome • ALS, encephalitis, brainstem stroke Quality of life, extreme social restriction • Other applications not yet imagined or designed
BCI (for kaiser’s notes only)
Team Projects EC1 baseline Search literature to EO1 baseline identify two tasks studied Task 1 by EEG or fMRI, and the complementary sites • Site 1 activates, Site 2 no change Task 2 • Site 1 no change, Site 2 activates EC2 baseline EO2 baseline Limitations: Macrostate, Alpha activity only, post- hoc artifact control
Dedicated to my family formaking everything worthwhile
READ not to contradict or confute Nor to Believe and Take for Granted but TO WEIGH AND CONSIDER THANK YOU My sincere thanks to MEDHA SRINVASANSECRETARY- SOCIETY FOR ADVANCEMENT OF BRAIN ANALYSIS- INDIAN CHAPTER