Its now over a month since my initial TDCs session. I have been distracted by academic studies. Today I will do the working memory protocol again and tomorrow the Math protocol. I still have not built the new device but would like to get that done next week.
I would also like to make a suitable DC bio current monitor. Many years ago there was a gentleman selling a German DC bio current monitor. It was perhaps 15 years ago & I have forgotten the brand name. It should be a relatively easy device to construct but I would like to code a JAVA PC interface also.
Monday, 27 August 2012
Monday, 13 August 2012
In the flow on working memory training today
Today I did another working memory N-Back training session. Definitely more in the flow than normal. Making less conscious effort to recall selections. Did have an issue with humidity & sweat causing an electrode to fall off at first.
Thursday, 9 August 2012
Combining TDCs with fNIRS Hemoencephalography for Working Memory
Hemoencephalography is a form of biofeedback that employs fNIRS infra red LEDs to project light through the skull into the brain. The light is then reflected back to detectors & reveals the blood flow to the brain surface.
This is most commonly used on the prefrontal cortex where working memory is localized. Research reveals that the strength of links between the prefrontal cortex and other brain structures are an indicator of intelligence http://news.wustl.edu/news/Pages/24068.aspx
Control of thought and behavior is fundamental to human intelligence. Evidence suggests a frontoparietal brain network implements such cognitive control across diverse contexts. We identify a mechanism—global connectivity—by which components of this network might coordinate control of other networks. A lateral prefrontal cortex (LPFC) region's activity was found to predict performance in a high control demand working memory task and also to exhibit high global connectivity. Critically, global connectivity in this LPFC region, involving connections both within and outside the frontoparietal network, showed a highly selective relationship with individual differences in fluid intelligence. These findings suggest LPFC is a global hub with a brainwide influence that facilitates the ability to implement control processes central to human intelligence.
As HEG is non electrical and even less invasive than TDCs there is no interference between the two modalities if used at the same time.
By combining HEG biofeedback and TDCs one should be able to generate a more significant progression with working memory training. Both Working Memory and prefrontal cortex biofeedback are linked to cognitive enhancement and increases in IQ.
HEG devices are very easy to construct simply consisting of an array of infra red LEDs with the correct bandwidth to be responsive to blood cells. The software is more challenging for non programmers but I am a JAVA developer & electronics engineer so I am comfortable with the project.
The data is processed and interfaced with biofeedback software.
Last year I researched fNIRS and found a site showing how to make a device in some detail especially how to make the head set from silicone, sensors & LED's. Unfortunately a search of my HDD has failed to come up with the link. Really such a device is easy to construct with optical fibres running to the the signal processing box .http://felixchenier.com/lib/exe/fetch.php?media=research:pdf:a_new_brain_imaging_device_based_on_fnirs.pdf Discusses some of the hardware.
As a final observation if we look at the Drexel page outling areas of fNIRS research http://www.biomed.drexel.edu/fnir/CONQUER/fNIR_Research.html we can see that there is a strong overlap with TDCs research of most interest math ability and general cognitive enhancement.
Wednesday, 8 August 2012
Principles of Memory & Neuroplasticity
1. "Interest" – In order to remember something thoroughly, you must be interested in it. You must
have a reason to learn it. Seek ways to make it personal.
2. "Intent to Remember" – has much to do with whether or not you remember something. A
key factor to remembering is having a positive attitude that you will remember. Take notes.
Predict test questions. Use a concentration checklist; every time your mind wanders, put a check
on this sheet. Eventually, you will program your mind to pay attention.
3. "Basic Background"( – Your understanding of new material depends, to a great degree, on
how much you already know about the subject. The more you increase your basic knowledge, the
easier it is to build new knowledge on this background. Before reading an assignment, preview it.
Try to recall what you already know.
4. "Selectivity"– You must determine what is most important, and select those parts to study and
learn. You cannot remember everything about everything. Look for verbal and non-verbal clues
during lecture. Make flashcards. Devise sample tests.
5. "Meaningful Organization" – You can learn and remember better if you group ideas into
meaningful categories. Search for ways to organize information into categories that are
meaningful to you. Alphabetize a list. Use a variety of mnemonic devices.
6. "Recitation" – Saying ideas aloud in your own words is one of the most powerful tools you
have to transfer information from short-term to long-term memory. When you finish reading a
paragraph/section in a textbook, stop and recite.
7. "Mental Visualization" – Another powerful memory principle is making a mental picture of
what needs to be remembered. By visualizing, you use an entirely different part of the brain than
you do when reading or listening.
8. "Association" – Memory is increased when facts to be learned are associated with something
familiar to you. By recalling something you already know and making a link to the "brain file"
that contains that information, you should be able to remember new information more efficiently.
9. "Consolidation" – Your brain must have time for new information to soak in. Take notes and
review them. Ask questions. Make flashcards. Make practice tests.
10."Distributed Practise"– A series of shorter study sessions distributed over several days is
preferable to fewer, but longer study sessions. After each hour of study, take a 10-minute break.
Have a scheduled time to study each subject. Make use of daylight hours and time you usually
waste. Study immediately before and after class. Review. Review. Review!
"Don't forget the curve of forgetting"
12 more principles of memory:
Selectivity
Association
Visualization
Elaboration
Concentration
Recitation
Intention
Big & Little pictures
Feedback
Organization
Time on Task
Ongoing Review
Four More:
Practice Retrieval
Process Material Actively
Use Distributed Practise
Use Metamemory
Specifics: Eidetics, Mnemonics, Chunking, Linking, Synaesthesia
Neuroplasticity
• Synaptic connections are continually being modified (re-organisation of
circuitry)
– In response to demand – learning, memory, disuse
– After damage to the CNS
– LTP: alteration of the structure of the synapse
• Cellular level
– Increased sensitivity to neural transmitters
– Increase number and branches of dendrites
– Increase and strengthening of synaptic connections (Hebbe)
– Axon sprouting
Cortical maps – ‘use it or lose it’
"CONSTRAINT & REINFORCEMENT"
By constraining an appropriate behaviour and reinforcing another the underlying brain structure will modify its neural function to perform the reinforced task & not the constrained one.
i. The Effect of Use on Neural Substrates
The first principle of neuroplasticity is that if a neural substrate is not biologically active, it will degrade in function.
ii. Usage Improves Function
This principle, an extension of the first, states that with increased biological activity, future functioning can be enhanced.
iii. Plasticity is Experience Specific
This principle suggests that changes in neural function with practice may be limited to the specific function being trained.
iv. Repetition of Training
This principle states that changes in neural substrates will occur only as a result of extensive and prolonged practice and that neural changes may not become consolidated until later in the training process.
v. Intensity of Training
The principle that training must be continuous over long periods to induce neural change.
vi. The Time of Training Onset
This principle states that different forms of neural plasticity may occur at various times in response to treatment.
vii. Salience of Training
The principle that training must be sufficiently salient to induce plasticity may be of considerable importance to speech. That is, simple repetitive movements or strength training may not enhance skilled movement and may have less potential for inducing changes in neural function underlying voice and speech production for communication.
viii. Age Effects on Training
Although neural plasticity can occur over the entire lifespan, it is well recognized that training and environmentally induced plasticity occur more readily in younger than in older nervous systems.
(See Ergogenics below)
(See Ergogenics below)
ix. Transference
The principle of transference states that plasticity following training in one function may enhance related behaviors and has been studied both in animals and human rehabilitation.
x. Interference
The interference principle is that plasticity can cause changes in neural function, which may interfere with behaviors or skills.
Neuroplasticity Ergogenics:
Hormonal factors NGF, IGF
TDCs
Amino Acids
Personal Observation: Somnabulistic Hypnosis & dreaming prove that neuroplasticity can in fact be practically instantaneous. Age related factors are largely determined by alterable physiological parameters such as growth factors, circulation & neurotransmitter levels.
Personal Observation: Somnabulistic Hypnosis & dreaming prove that neuroplasticity can in fact be practically instantaneous. Age related factors are largely determined by alterable physiological parameters such as growth factors, circulation & neurotransmitter levels.
Monday, 6 August 2012
TDCs Visualization Training
I have had a break from TDCs for a few days. My next protocol to try will be for the visual system - in particular visualisation in the minds eye & eidetic memory. I am an artist and have very vivid visual imagery if uncontrolled quite often. I also have flashes of eidetic memory.
Eidetic memory is not some genetic gift of savants as the western media portrays it. In Japan children are trained in Eidetic memorisation methods at special schools.
In Germany advanced Autogenic Therapy trains the minds eye to visualise with extreme precision & clarity. Most of the schools of meditation also train visualisation. Deep trance Hypnosis can induce vivid sensory experiences in a post trance.
What's more every night you enter the realm of an inner perceptual environment when dreaming.
So essentially we have been trained "not" to have an imagination, which is kind of like being trained not to walk. Human culture is an odd thing.
In France in the last century there was a famous art teacher Horace Lecoq de Boisbaudran, he trained Rodin and dozens of famous French artists.
His method was based upon drawing, and painting from memory. All pupils were forbidden from using direct vision or any physical likeness to reproduce a subject. After the initial visual familiarisation it had to be done entirely from memory.
The interesting point is that all of his pupils developed Eidetic Memory within six month of gruelling training. Not just memory but a vivid imagination also.
Now today this is largely neglected by the lazy masses thanks to TV & camera's. So without the proper mental stimulation we lose our inner world.
Neuroscientists have discovered that the principle behind the phenomena is neuroplasticity. The very basis of TDCs.
De Boisbaudran, by forbidding the use of physical props or scenes was "constraining" that part of the nervous system. The brain adapted by reinforcing the neurons and brain centres that are the basis of visualisation. After a period of intense training the students brains adapted to the extent that they had Eidetic Memory & a fully functioning imagination.
Eventually I would like to train my self to do the same. In a day or two I will try TDCs to stimulate visual memory and imagery.
Eidetic memory is not some genetic gift of savants as the western media portrays it. In Japan children are trained in Eidetic memorisation methods at special schools.
In Germany advanced Autogenic Therapy trains the minds eye to visualise with extreme precision & clarity. Most of the schools of meditation also train visualisation. Deep trance Hypnosis can induce vivid sensory experiences in a post trance.
What's more every night you enter the realm of an inner perceptual environment when dreaming.
So essentially we have been trained "not" to have an imagination, which is kind of like being trained not to walk. Human culture is an odd thing.
In France in the last century there was a famous art teacher Horace Lecoq de Boisbaudran, he trained Rodin and dozens of famous French artists.
His method was based upon drawing, and painting from memory. All pupils were forbidden from using direct vision or any physical likeness to reproduce a subject. After the initial visual familiarisation it had to be done entirely from memory.
The interesting point is that all of his pupils developed Eidetic Memory within six month of gruelling training. Not just memory but a vivid imagination also.
Now today this is largely neglected by the lazy masses thanks to TV & camera's. So without the proper mental stimulation we lose our inner world.
Neuroscientists have discovered that the principle behind the phenomena is neuroplasticity. The very basis of TDCs.
De Boisbaudran, by forbidding the use of physical props or scenes was "constraining" that part of the nervous system. The brain adapted by reinforcing the neurons and brain centres that are the basis of visualisation. After a period of intense training the students brains adapted to the extent that they had Eidetic Memory & a fully functioning imagination.
Eventually I would like to train my self to do the same. In a day or two I will try TDCs to stimulate visual memory and imagery.
Thursday, 2 August 2012
Effective TDCs Tinnitus Protocols Undefined
I am still researching appropriate electrode placements for tinnitus treatment. I am not going to risk placing them in the wrong area so this may take some time.
Both hemispheres of the Dorso Lateral Prefrontal Cortex are commonly treated but this is a relatively large surface area.
From:http://www.tinnitusresearch.org/en/patients/newintinnitusresearch_en.php
Many different functional and structural imaging techniques have been used to identify structures in the central nervous system which are believed to play an important role in the pathophysiology of many forms of tinnitus.
The neuroimaging methods functional magnetic resonance (fMRI) and positron emission tomography (PET) enable to measure regional changes of cerebral blood flow, which in turn is an indirect measurement of neuronal activity. Electro- (EEG) and Magnetoencephalography (MEG) measure neuronal activity directly. Alterations in the central auditory pathways in tinnitus patients have been shown already 15 years ago. However it has been only very recently that neuroimaging studies have systematically been used to differentiate the different forms of tinnitus (unilateral versus bilateral, pure tone versus noise like, with more and less distress, with shorter and longer duration) (Schecklmann et al. 2011;Vanneste, Van de Heyning, & De Ridder 2011a;Vanneste, Van de Heyning, & De Ridder 2011b). It has been demonstrated that all these forms differ in their brain activity pattern, especially in non-auditory brain areas. Also for the first time brain activity changes related to acute tinnitus after noise trauma have been studied (Ortmann et al. 2011) and it has been found that these differ substantially from those in chronic tinnitus.EEG and MEG have revealed consistent results across many studies in the sense that in tinnitus the normal activity pattern in the auditory cortex is changed. In the auditory cortex of tinnitus patients alpha activity is reduced, whereas delta and gamma activity is increased. Successful treatment reverses these abnormalities, indicating that they represent the neuronal correlate of tinnitus loudness. Syst Neurosci. 2012;6:15. Epub 2012 Apr 9. Neuroimaging and neuromodulation: complementary approaches for identifying the neuronal correlates of tinnitus. "...In conclusion, these preliminary studies indicate that both anodal stimulation of the left auditory cortex and bifrontal tDCS with the cathode left and the anode right can have beneficial effects on tinnitus in some individuals. The interindividual variability of treatment effects is high in all studies, suggesting that there may be pathophysiologically distinct forms of tinnitus that respond particularly well to different tDCS protocols (Vanneste et al.,
2011c).
In order to unravel the mechanism by which tDCS suppresses tinnitus EEG
measurements were performed before and after single sessions of bifrontal tDCS
in 12 patients who responded to tDCS. Reduction of tinnitus intensity and
tinnitus-related distress was related to modulation of neuronal activity in
pregenual anterior cingulate cortex, parahippocampal area, and right primary
auditory cortex regions (Vanneste et al., 2011a). These findings are comparable
to those obtained in healthy controls after a similar tDCS intervention (anode
positioned over the left DLPFC and the cathode over the right supraorbital
region), that revealed a tDCS induced modulation of regional electrical activity
in the left subgenual prefrontal cortex, the anterior cingulate cortex and the
left parahippocampus (Keeser et al., 2011b) and significant changes of regional
brain connectivity both for the default mode network and the fronto-parietal
network (Keeser et al., 2011a)."
and diffusion tensor imaging.
Abstract
INTRODUCTION: Tinnitus is a poorly understood auditory perception of sound in
the absence of external stimuli. Convergent evidence proposes that tinnitus
perception involves brain structural alterations as part of its pathophysiology.
The aim of this study is to investigate the structural brain changes that might
be associated with tinnitus-related stress and negative emotions.
METHODS: Using high-resolution magnetic resonance imaging and diffusion tensor
imaging, we investigated grey matter and white matter (WM) alterations by
estimating cortical thickness measures, fractional anisotropy and mean
diffusivity in 14 tinnitus subjects and 14 age- and sex-matched non-tinnitus
subjects.
RESULTS: Significant cortical thickness reductions were found in the prefrontal
cortex (PFC), temporal lobe and limbic system in tinnitus subjects compared to
non-tinnitus subjects. Tinnitus sufferers were found to have disrupted WM
integrity in tracts involving connectivity of the PFC, temporal lobe, thalamus
and limbic system.
CONCLUSION: Our results suggest that such neural changes may represent neural
origins for tinnitus or consequences of tinnitus and its associations.
Some research:http://proceedings.ebea2011.org/modules/request205f.pdf?module=oc_program&action=view.php&id=5178
Bifrontal transcranial direct current stimulation (tDCS), with the anodal electrode overlying the right and the cathodal electrode overlying the left dorsolateral prefrontal cortex, has been shown to suppress tinnitus significantly in 30% of patients.
So there are various types of tinnitus with different neurological correlates. On top of this there are individual brain structures and neural layouts. At present the research is ongoing and a partial reduction of symptoms in 30% of subjects is not sufficient for me to undertake TDCs for Tinnitus as of this time.
Both hemispheres of the Dorso Lateral Prefrontal Cortex are commonly treated but this is a relatively large surface area.
From:http://www.tinnitusresearch.org/en/patients/newintinnitusresearch_en.php
Many different functional and structural imaging techniques have been used to identify structures in the central nervous system which are believed to play an important role in the pathophysiology of many forms of tinnitus.
The neuroimaging methods functional magnetic resonance (fMRI) and positron emission tomography (PET) enable to measure regional changes of cerebral blood flow, which in turn is an indirect measurement of neuronal activity. Electro- (EEG) and Magnetoencephalography (MEG) measure neuronal activity directly. Alterations in the central auditory pathways in tinnitus patients have been shown already 15 years ago. However it has been only very recently that neuroimaging studies have systematically been used to differentiate the different forms of tinnitus (unilateral versus bilateral, pure tone versus noise like, with more and less distress, with shorter and longer duration) (Schecklmann et al. 2011;Vanneste, Van de Heyning, & De Ridder 2011a;Vanneste, Van de Heyning, & De Ridder 2011b). It has been demonstrated that all these forms differ in their brain activity pattern, especially in non-auditory brain areas. Also for the first time brain activity changes related to acute tinnitus after noise trauma have been studied (Ortmann et al. 2011) and it has been found that these differ substantially from those in chronic tinnitus.EEG and MEG have revealed consistent results across many studies in the sense that in tinnitus the normal activity pattern in the auditory cortex is changed. In the auditory cortex of tinnitus patients alpha activity is reduced, whereas delta and gamma activity is increased. Successful treatment reverses these abnormalities, indicating that they represent the neuronal correlate of tinnitus loudness. Syst Neurosci. 2012;6:15. Epub 2012 Apr 9. Neuroimaging and neuromodulation: complementary approaches for identifying the neuronal correlates of tinnitus. "...In conclusion, these preliminary studies indicate that both anodal stimulation of the left auditory cortex and bifrontal tDCS with the cathode left and the anode right can have beneficial effects on tinnitus in some individuals. The interindividual variability of treatment effects is high in all studies, suggesting that there may be pathophysiologically distinct forms of tinnitus that respond particularly well to different tDCS protocols (Vanneste et al.,
2011c).
In order to unravel the mechanism by which tDCS suppresses tinnitus EEG
measurements were performed before and after single sessions of bifrontal tDCS
in 12 patients who responded to tDCS. Reduction of tinnitus intensity and
tinnitus-related distress was related to modulation of neuronal activity in
pregenual anterior cingulate cortex, parahippocampal area, and right primary
auditory cortex regions (Vanneste et al., 2011a). These findings are comparable
to those obtained in healthy controls after a similar tDCS intervention (anode
positioned over the left DLPFC and the cathode over the right supraorbital
region), that revealed a tDCS induced modulation of regional electrical activity
in the left subgenual prefrontal cortex, the anterior cingulate cortex and the
left parahippocampus (Keeser et al., 2011b) and significant changes of regional
brain connectivity both for the default mode network and the fronto-parietal
network (Keeser et al., 2011a)."
Neuroanatomical correlates of tinnitus revealed by cortical thickness analysisNeuroanatomical correlates of tinnitus revealed by cortical thickness analysis anddiffusion tensor imaging. Abstract INTRODUCTION: Tinnitus is a poorly understood auditory perception of sound in the absence of external stimuli. Convergent evidence proposes that tinnitus perception involves brain structural alterations as part of its pathophysiology. The aim of this study is to investigate the structural brain changes that might be associated with tinnitus-related stress and negative emotions. METHODS: Using high-resolution magnetic resonance imaging and diffusion tensor imaging, we investigated grey matter and white matter (WM) alterations by estimating cortical thickness measures, fractional anisotropy and mean diffusivity in 14 tinnitus subjects and 14 age- and sex-matched non-tinnitus subjects. RESULTS: Significant cortical thickness reductions were found in the prefrontal cortex (PFC), temporal lobe and limbic system in tinnitus subjects compared to non-tinnitus subjects. Tinnitus sufferers were found to have disrupted WM integrity in tracts involving connectivity of the PFC, temporal lobe, thalamus and limbic system. CONCLUSION: Our results suggest that such neural changes may represent neural origins for tinnitus or consequences of tinnitus and its associations.
and diffusion tensor imaging.
Abstract
INTRODUCTION: Tinnitus is a poorly understood auditory perception of sound in
the absence of external stimuli. Convergent evidence proposes that tinnitus
perception involves brain structural alterations as part of its pathophysiology.
The aim of this study is to investigate the structural brain changes that might
be associated with tinnitus-related stress and negative emotions.
METHODS: Using high-resolution magnetic resonance imaging and diffusion tensor
imaging, we investigated grey matter and white matter (WM) alterations by
estimating cortical thickness measures, fractional anisotropy and mean
diffusivity in 14 tinnitus subjects and 14 age- and sex-matched non-tinnitus
subjects.
RESULTS: Significant cortical thickness reductions were found in the prefrontal
cortex (PFC), temporal lobe and limbic system in tinnitus subjects compared to
non-tinnitus subjects. Tinnitus sufferers were found to have disrupted WM
integrity in tracts involving connectivity of the PFC, temporal lobe, thalamus
and limbic system.
CONCLUSION: Our results suggest that such neural changes may represent neural
origins for tinnitus or consequences of tinnitus and its associations.
http://www.springerlink.com/content/d67t81vx500870l2/Some research:http://proceedings.ebea2011.org/modules/request205f.pdf?module=oc_program&action=view.php&id=5178
Bifrontal transcranial direct current stimulation (tDCS), with the anodal electrode overlying the right and the cathodal electrode overlying the left dorsolateral prefrontal cortex, has been shown to suppress tinnitus significantly in 30% of patients.
So there are various types of tinnitus with different neurological correlates. On top of this there are individual brain structures and neural layouts. At present the research is ongoing and a partial reduction of symptoms in 30% of subjects is not sufficient for me to undertake TDCs for Tinnitus as of this time.
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