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Electrodes in the brain and 'repetitive orgasms'

Electrodes in the brain and 'repetitive orgasms'


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The advent of chlorpromazine in 1955 put an end to one of the more bizarre chapters in American psychiatry.$^1$ Dr. Robert Heath implanted wires or delivered injections of acetylcholine (a neurotransmitter) deep into the 'septal regions' of the brains of men and women with various physical and mental disorders. His discovery of the brain's 'pleasure center' actually preceded the discovery of the same center in rats by about 20 years [Baumeister, below, at 272].

In one of his papers$^2$ Heath describes intense orgasmic experiences on the part of his patients in response to his treatments, which he dutifully records on EEGs.

His description of Patient b-5 is especially interesting. He relates: "The patient became more attuned to her environment, answered questions more rapidly and accurately, and solved simple mathematical problems with more ease… and in most instances, within another 5 to 10 minutes, this [heightened attunement] culminated in repetitive orgasms." [Heath, below, at 12].

In addition to refreshing my interest in solving simple mathematical problems, this article made me wonder whether this area of research had been resumed in some form. Many of the ethical and technical problems discussed in Maumeister's article seem surmountable, especially in light of computer-aided visualization of brain structures. Not to mention that a kindred treatment, ECT (electroshock), which can still actually be done involuntarily, has seen something of a comeback in the U.S. since the 1940s. ECT is basically controlled destruction of brain tissue, which seems to cast Heath's work in a kinder light.

So my question is whether this thread has been taken up or whether, as one VIP put it, the absence of evidence is evidence of absence. I was unable to turn anything up.

Thanks for any enlightenment.

$^1$ Baumeister, The Tulane Electrical Brain Stimulation Program: A Historical Case Study in Medical Ethics (2000), J. of the History of the Neurosciences 9 (3): 262-78. See page 270.

$^2$Heath, Pleasure and Brain Activity in Man, (1972) Journal of Nervous and Mental Disease 154 (1): 3-17.


The Fascinating World of Your Brain's Reward System

Many people think that the brain’s reward system is the part of the brain that causes addictions. However, there’s one essential aspect that we have to understand here. Having goals is synonymous with health and well-being. Thus, all of this neurobiology, which is behind the motivation and pleasure you find in your daily life, is regulated by this complex, yet fascinating, group of neural structures.

Eating, resting, drinking a cup of coffee with friends, waiting for a like on the photo you’ve just uploaded, eating a chocolate-filled dessert, going shopping, or going or to the cinema… These common daily situations are all governed by your brain’s reward system.

Often, when we talk about this neural structure, it’s common to hear that its most basic priority is to ensure our survival. All the processes carried out by primordial instinct are automatic. They’re governed, in most cases, by a very basic emotion: fear. This emotion makes you prudent and careful. It reminds you of the dangers in life and it tells you that it’s often best to stay safe in your comfort zone.


Introduction

An ongoing challenge confronting basic scientists, as well as those at the translational interface, is the ability to access a rapid and cost-effective tool to uncover mechanistic details of neural function and dysfunction. For example, identifying the presence of stroke, establishing altered neural dynamics in traumatic brain damage, and monitoring changes in neural profile in athletes on the sidelines all pose major hurdles. In this paper, using scalp electroencephalography (EEG) signals with relatively little data, we provide theoretical and empirical support for a method for the noninvasive detection of neural silences. We adopt the term silences or regions of silence to refer to the areas of brain tissue with little or no neural activity. These regions reflect ischemic, necrotic, or lesional tissue, resected tissue (e.g., after epilepsy surgery), or tumors 1,2 . Dynamic regions of silence also arise in cortical spreading depolarizations (CSDs), which are slowly spreading waves of silences in the cerebral cortex 3,4,5 .

There has been growing utilization of EEG for diagnosis and monitoring of neurological disorders such as stroke 6 , and concussion 7 . Common imaging methods for detecting brain damage, e.g., magnetic resonance imaging (MRI) 8,9 , or computed tomography 10 , are not portable, are not designed for continuous (or frequent) monitoring, are difficult to use in many emergency situations, and may not even be available at medical facilities in many countries. However, many medical scenarios can benefit from portable, frequent/continuous monitoring of neural silences, e.g., detecting changes in tumor or lesion size/location and CSD propagation. Noninvasive scalp EEG is, however, widely accessible in emergency situations and can even be deployed in the field with only a few limitations. It is easy and fast to setup, portable, and of lower cost compared with other imaging modalities. Additionally, unlike MRI, EEG can be recorded from patients with implanted metallic objects in their body, e.g., pacemaker 11 .

Source vs. silence localization

An ongoing challenges of EEG is source localization, the process by which the location of the underlying neural activity is determined from the scalp EEG recordings. The challenge arises primarily from three issues: (i) the underdetermined nature of the problem (few sensors, many possible locations of sources) (ii) the spatial low-pass filtering effect of the distance and the layers separating the brain and the scalp and (iii) noise, including exogenous noise, background brain activity, as well as artifacts, e.g., heart beats, eye movements, and jaw clenching 12,13 . In source localization paradigms applied to neuroscience data 14,15,16 , e.g., in event-related potential paradigms 17,18 , scalp EEG signals are aggregated over event-related trials to average out background brain activity and noise, permitting the extraction of the signal activity that is consistent across trials. The localization of a region of silence poses additional challenges, of which the most important is how the background brain activity is treated: while it is usually grouped with noise in source localization (e.g., authors in 16 state: “EEG data are always contaminated by noise, e.g., exogenous noise and background brain activity”), estimating where background activity is present is of direct interest in silence localization where the goal is to separate normal brain activity (including background activity) from abnormal silences. Because source localization ignores this distinction, as we demonstrate in our experimental results below, classical source localization techniques, e.g., multiple signal classification (MUSIC) 19,20 , minimum norm estimation (MNE) 15,21,22,23 , and standardized low-resolution brain electromagnetic tomography (sLORETA) 24 , even after appropriate modifications, fail to localize silences in the brain (“Methods” details our modifications on these algorithms).

To avoid averaging out the background activity, we estimate the contribution of each source to the recorded EEG across all electrodes. This contribution is measured in an average power sense, instead of the mean, thereby retaining the contributions of the background brain activity. Our silence localization algorithm, referred to as SilenceMap, estimates these contributions, and then uses tools that quantify our assumptions on the region of silence (contiguity, small size of the region of silence, and being located in only one hemisphere) to localize it. Because of this, another difference arises: silence localization can use a larger number of time points (than typical source localization). For example, 160 s of data with the sampling frequency of 512 Hz provides SilenceMap with around 81,920 data points to be used, boosting the signal-to-noise ratio (SNR) over source localization techniques, which typically rely on only a few tens of event-related trials to average over and extract the source activity that is consistent across trials.

Further, we confront two additional difficulties: lack of statistical models of background brain activity, and the choice of the reference electrode. The first is dealt with either by including baseline recordings (in absence of silence which we did not have for our experimental results) or utilizing a hemispheric baseline, i.e., an approximate equality in power measured at electrodes placed symmetrically with respect to the longitudinal fissure (see Fig. 1b). While the hemispheric baseline used here provides fairly accurate reconstructions, we note that this baseline is only an approximation, and an actual baseline is expected to further improve the accuracy. The second difficulty is related: to retain this approximate hemispheric symmetry in power, it is best to utilize the reference electrode on top of the longitudinal fissure (see Fig. 1a). Using these advances, we propose an iterative algorithm to localize the region of silence in the brain using a relatively small amount of data. In simulations and real data analysis, SilenceMap outperformed existing algorithms in localization accuracy for localizing silences in three participants with surgical resections using only 160 s of EEG signals across 128 electrodes (see “Results” for more details on finding the minimum amount of EEG data for localizing silences using SilenceMap).

a The EEG recording protocol and the locations of scalp electrodes. One of 10 reference electrodes (shown in red) is chosen along the longitudinal fissure for rereferencing against. b Average power of scalp potentials for different choices of reference electrodes. c Symmetric brain model of a patient (UD) with a right occipitotemporal lobectomy. d Steps of SilenceMap in a low-resolution source grid. A measure of the contribution of brain sources in the recorded scalp signals ( ( ilde<eta >) ) is calculated relative to a hemispheric baseline. In the brain colormap, yellow indicates no contribution. A contiguous region of silence is localized based on a convex spectral clustering (CSpeC) framework in the low-resolution grid. e Steps of SilenceMap in a high-resolution source grid. The source covariance matrix (Cs) is estimated through an iterative method, and the region of silence is localized using the CSpeC framework. f Choosing the best reference electrode to reference against (Cz in this example), which results in minimum scalp power mismatch (ΔPow). The localized region of silence for this patient (UD) has 13 mm COM distance (ΔCOM) from the original region, with more than 38% overlap (JI = 0.384), and it is 32% smaller (Δk = 0.32).


Effects of repetitive paired associative stimulation on brain plasticity and working memory in Alzheimer’s disease: a pilot randomized double-blind-controlled trial

Pilot randomized double-blind-controlled trial of repetitive paired associative stimulation (rPAS), a paradigm that combines transcranial magnetic stimulation (TMS) of the dorsolateral prefrontal cortex (DLPFC) with peripheral median nerve stimulation.

To study the impact of rPAS on DLPFC plasticity and working memory performance in Alzheimer’s disease (AD).

Thirty-two patients with AD (females = 16), mean (SD) age = 76.4 (6.3) years were randomized 1:1 to receive a 2-week (5 days/week) course of active or control rPAS. DLPFC plasticity was assessed using single session PAS combined with electroencephalography (EEG) at baseline and on days 1, 7, and 14 post-rPAS. Working memory and theta–gamma coupling were assessed at the same time points using the N-back task and EEG.

There were no significant differences between the active and control rPAS groups on DLPFC plasticity or working memory performance after the rPAS intervention. There were significant main effects of time on DLPFC plasticity, working memory, and theta–gamma coupling, only for the active rPAS group. Further, on post hoc within-group analyses done to generate hypotheses for future research, as compared to baseline, only the rPAS group improved on post-rPAS day 1 on all three indices. Finally, there was a positive correlation between working memory performance and theta–gamma coupling.


How Binaural Beats Affect Your Brain – and How They Don’t

T he beat is low and steady &ndash but it&rsquos all just in my head&hellip While I&rsquom sitting on my couch, listening to some smooth jazz, there is a faint beat in the background. It doesn&rsquot seem remarkable &ndash except for the fact that I can&rsquot hear the beat from my headphones. Instead, I sense it in the center of my brain.

Binaural beats are like optical illusions for sounds. When your left ear hears a slightly different tone from your right ear, you perceive a beat not present in the music you listen to. These binaural beats (from Latin &ldquowith both ears&rdquo) have been peddled as &ldquodigital drugs&rdquo, producing all sorts of effects from improving sleep to enhancing your memory.

For example, recently the pharmaceutical company Bayer, manufacturer of Aspirin, put seven files of binaural beats on its Austrian website. The idea: by making you relax, the beats may put you in a relaxed state, which could alleviate headaches. But it is far from certain whether this idea &ndash and many others about binaural beats &ndash hold true.

The binaural beat percept
Let&rsquos take a loudspeaker. We&rsquoll play two sine waves, one with a frequency of 440 Hertz (cycles per seconds) and one of 446 Hertz. The sound travels to your ear and the two waves interact with each other, either cancelling each other out or amplifying each other. The sound waxes and wanes periodically: this is called a beat, specifically a monaural beat.

Two waves of different frequencies (red and blue signals) added to create a third signal (bottom panel, pink). This new signal contains a 6 Hz beat (e.g., a 6 cycle per second rhythm). The red and blue signals and also show behind the new signal.

The frequency of the beat is equal to the differences in frequency between the two original sine waves &ndash in this case, 6 Hertz.

Now, let&rsquos take a set of headphones. We&rsquoll split the two waves, and play a sine wave of 440 Hertz in your left ear and a sine wave of 446 Hertz in your right ear. Now, what do you hear?

Again, you&rsquoll hear a beat of 6 Hertz. But now there is no room for the two waves to physically interact &ndash it is all in your head. While monaural beats can be heard when you listen with both ears, one ear is enough to perceive them (hence &ldquomonaural&rdquo from the Latin phrase &ldquowith one ear&rdquo). Binaural beats, however, can only be perceived with both ears, hence their name derives from &ldquowith both ears&rdquo. They also differ in how you perceive them: monaural beats pulse from very loud to silent, while binaural beats only change slightly in volume.

We still do not know for sure which brain regions are involved in generating the binaural beat percept. A part of the brain called the superior olivary nucleus may be one such region, but this is not yet certain.

    • Sample clip of a binaural beatBinaural-Beat-Clip 1.mp3 (Disclaimer: Please consult your doctor before listening to binaural beats if you suffer from any neurological disease or have had a stroke.)

    Heinrich Wilhelm Dove, a German experimenter, first discovered binaural beats in 1839. Much of what we know about binaural beats comes from an article by Gerald Oster, published in Scientific American in 1973. Oster envisioned binaural beats as a tool in research and medicine, allowing researchers to investigate the neuronal basis of hearing.

    He might be surprised if he did a quick Google search to see what binaural beats are used for today. A whole industry has been built on the illusion (as we&rsquoll see) that binaural beats improve your wellbeing. These claims range from helping you meditate, increasing your IQ, making you relax and sleep, promoting creativity, reducing anxiety, to activating your self-healing abilities.

    In September, the pharmaceutical company Bayer released seven tracks of binaural beats on its Austrian website. Presented under the title &ldquoGood Vibes for our brain &ndash powered by Aspirin&rdquo, the website proposes that binaural beats are &ldquoa pleasant and easy way to e.g. alleviate headaches through relaxation&rdquo.

    &ldquoBut do binaural beats really affect brain waves?&rdquo

    Bayer presents the tracks very cautiously (my emphasis): the &ldquolow-frequency sound may influence brain waves. [&hellip] Frequencies between 8-14 Hertz are called alpha waves, and occur mostly during a relaxed state. [&hellip] The resulting difference [frequency of our beat] is 10 Hertz. Thereby, alpha waves should be generated, which help to bring the listener into a relaxed state. A pleasant and easy way to e.g. alleviate headaches through relaxation.&rdquo

    So note that Bayer Austria does not actually claim that binaural beats help headaches, merely that they may help you relax. But let&rsquos breakdown the different parts of their statement.

    Brain waves and binaural beats
    Firstly, the brain waves. Brain waves are the neural oscillations seen on an EEG Electroencephalogram, a technique that places electrodes on . recording. In short, the EEG reflects the activity of many neurons, and is recorded noninvasively from the scalp. Sometimes, whole groups of neurons are active at the same time, and this can be seen as brain waves on the EEG. Different frequencies are associated with different tasks or mental states.

    Gamma waves, which oscillate at 30-100 cycles per second, are associated with memory and attention. Alpha waves, at 8-12 cycles per second (or Hertz), are associated with an idle, restful state. When your eyes are shut and you are resting, your EEG would likely show up as alpha waves. Most websites trying to sell you &ldquoexclusive binaural beats&rdquo will tell you that their beats influence your brain waves, shifting them to a desired frequency and thus inducing that state, e.g., relaxation or memory. But do binaural beats really affect brain waves?

    &ldquoMen and women may perceive binaural beats differently, and perception may change throughout the menstrual cycle.&rdquo

    One way in which binaural beats may influence brain waves is through entrainment. Entrainment here means that the activity of your EEG becomes similar to a certain frequency set by an external stimulus. An example of entrainment is repetitive clicks: if you hear clicks at a certain frequency, your EEG is likely to show waves at this same frequency.

    Another way binaural beats may influence your brain waves is through phase synchronization Coordination in time between components of a system such as . . It has been suggested, but not thoroughly tested, that auditory beats increase the synchronization of the phase of brain waves in different brain regions.

    One study tested the effect of binaural beats on EEG rhythms in epilepsy A nervous system disorder that causes seizures due to abnorm. patients. In some hard-to-treat cases of epilepsy, patients are implanted with electrodes to pinpoint exactly where in their brain a seizure An event that is associated with uncontrolled and excessive . starts (to stop seizures, this area can then be removed). In this study, 10 epilepsy patients were implanted with intracranial electrodes, and the researchers recorded their EEG response to both monaural and binaural beats to see how the beats influence brain waves.

    The researchers found that beats can modulate oscillations and phase synchronization. But for binaural beats, they mostly observed a decrease in EEG power and phase synchronization. This means that there are weaker brain waves at the frequency of the beat, and the EEG phases across the brain fall more out of sync. Only when the patients listened to 10 Hz and 40 Hz binaural beats did EEG power increase, i.e., there were stronger brain waves at these frequencies. This entrainment had previously been described for 40 Hz binaural beats .

    But will binaural beats make your headache go away? You can test it on yourself when your head hurts next time &ndash but science says: we just don&rsquot know, yet.

    Binaural beats are not digital drugs
    Now, could this entrainment really have an effect on your memory, creativity or pain perception? It is probably safest to say that the jury is still out on this question. A 2015 review of the available literature summarized several studies on the effect of binaural beats on memory, creativity, attention, anxiety, mood and vigilance. The authors concluded that for most of these applications, findings are either contradictory or only supported by a single study. The only consistent finding was that several studies reported that binaural beat stimulation reduces anxiety levels. How anxiety is reduced, however, is not yet understood.

    One study suggested that binaural beats may increase relaxation after exercise. However, the subjects in this study listened to binaural beats in the theta range, 4-7 Hertz . Another study reported that study participants subjectively rated pain lower after they listened to binaural beats at 8, 10 and 12 Hertz, i.e., in the alpha range. So while there is no definite proof that binaural beats increase relaxation or reduce pain, further research may back this idea up.

    And this is the problem with binaural beat research &ndash we still do not know how the illusion of binaural beats is generated in our brains, or which brain networks are affected by them. If we knew, experimental standards could be harmonized and optimized to probe and report the effects of binaural beats more accurately. As it is, protocols vary widely between different studies &ndash from which wave ranges are tested to how long subjects listen to beats and what background frequencies are used. All of these may impact the effect of binaural beats on brain waves, mood or pain &ndash but we don&rsquot know it.

    Just a few examples of how funny these beats are: older people can detect beats in the gamma range, but not as accurately as younger people. Men and women may perceive binaural beats differently, and perception may change throughout the menstrual cycle. Given that we can&rsquot explain these observations, we need to properly understand binaural beats before we can probe their effect. And yes, music might help you relax, and this might improve your headache &ndash or mood, anxiety, creativity, or sleep. But will binaural beats make your headache go away? You can test it on yourself when your head hurts next &ndash but science says: we just don&rsquot know, yet.

    References:

    Oster: Auditory beats in the brain. In: Scientific American. 1973 Oct 229(4):94-102

    Becher et al. Intracranial electroencephalography power and phase synchronization changes during monaural and binaural beat stimulation. Eur J Neurosci. 2015 Jan41(2):254-63

    Chaieb et al. Auditory Beat Stimulation and its Effects on Cognition and Mood States. Front Psychiatry. 2015 6: 70.

    Image by Kayleen Schreiber


    Neurophysiological investigations

    Geraint Fuller MA MD FRCP , Mark Manford BSc MBBS MD FRCP , in Neurology (Third Edition) , 2010

    Sensitivity and specificity of paroxysmal interictal EEG discharges

    The EEG has a relatively low sensitivity and a higher specificity for the diagnosis of epilepsy. The results depend heavily on the population being tested. The false-positive rate of epileptiform interictal EEG abnormalities (epileptiform EEG changes in individuals who definitely do not have epilepsy) is 0.5–2% of randomly selected individuals and 5–10% of first-degree relatives of patients with epilepsy. The first EEG may show epileptiform changes in 50% of patients with definite epilepsy. A sleep-deprived EEG increases the diagnostic yield to 75% and repeating the EEG up to 80%. As many as 15% of patients with epilepsy consistently have a normal interictal EEG.


    Brain chemical potential new hope in controlling Tourette Syndrome tics

    A chemical in the brain plays a vital role in controlling the involuntary movements and vocal tics associated with Tourette Syndrome (TS), a new study has shown.

    The research by psychologists at The University of Nottingham, published in the latest edition of the journal Current Biology, could offer a potential new target for the development of more effective treatments to suppress these unwanted symptoms.

    The study, led by PhD student Amelia Draper under the supervision of Professor Stephen Jackson, found that higher levels of a neurochemical called GABA in a part of the brain known as the supplementary motor area (SMA) helps to dampen down hyperactivity in the cortical areas that produce movement.

    By reducing this hyperactivity, only the strongest signals would get through and produce a movement.

    Amelia said: "This result is significant because new brain stimulation techniques can be used to increase or decrease GABA in targeted areas of the cortex. It may be possible that such techniques to adjust the levels of GABA in the SMA could help young people with TS gain greater control over their tics."

    Tourette Syndrome is a developmental disorder associated with these involuntary and repetitive vocal and movement tics. Although the exact cause of TS is unknown, research has shown that people with TS have alterations in their brain 'circuitry' that are involved in producing and controlling motor functions.

    Both the primary motor cortex (M1) and the supplementary motor area (SMA) are thought to be hyperactive in the brains of those with TS, causing the tics which can be both embarrassing and disruptive, especially for children who often find it difficult to concentrate at school.

    Tics can be partially controlled by many people with TS but this often takes enormous mental energy and can leave them exhausted towards the end of the day and can often make their tics more frequent and excessive when they 'relax'. The majority of people diagnosed with TS in childhood manage to gain control over their tics gradually until they have only mild symptoms by early adulthood but this is often too late for some people who have had their education and social friendships disrupted.

    The scientists used a technique called magnetic resonance spectroscopy (MRS) in a 7 Tesla Magnetic Resonance Imaging (MRI) scanner to measure the concentration of certain chemicals in the brain known as neurotransmitters which offer an indication of brain activity.

    The chemicals were measured in the M1, the SMA and an area involved in visual processing (V1) which was used as a control (comparison) site. They tested a group of young people with TS and a matched group of typical young people with no known disorders.

    They discovered that the people with TS had higher concentrations of GABA, which inhibits neuronal activity, in the SMA.

    They used other neuroscience techniques to explore the result in greater detail, finding that having more GABA in the SMA meant that the people with Tourette Syndrome had less activity in the SMA when asked to perform a simple motor task, in this case tapping their finger, which they were able to measure using functional MRI.

    Using another technique called transcranial magnetic stimulation (TMS) in which a magnetic field is passed over the brain to stimulate neuron activity, they found that those with the most GABA dampen down the brain activity in the M1 when preparing to make a movement. In contrast, the typically developing group increased their activity during movement preparation.

    Finally, they considered how GABA was related to brain structure, specifically the white matter fibre bundles that connect the two hemispheres of the brain, a structure called the corpus callosum. They discovered that those with the highest levels of GABA also had the most connecting fibres, leading them to conclude that the more connecting fibres there are then the more excitatory signals are being produced leading to the need for even more GABA to calm his excess hyperactivity.

    The results could lead the way to more targeted approaches to controlling tics. New brain techniques such as transcranial direct-current stimulation (tdcs), a form of neurostimulation which uses constant, low level electrical current delivered directly to the brain via electrodes, has already been shown to be successful in increasing or decreasing GABA in targeted areas of the cortex.

    Professor Stephen Jackson added: "This finding is paradoxical because prior to our finding, most scientists working on this topic would have thought that GABA levels in TS would be reduced and not increased as we show. This is because a distinction should be made between brain changes that are causes of the disorder (e.g., reduced GABA cells in some key brain areas) and secondary consequences of the disorder (e.g., increased release of GABA in key brain areas) that act to reduce the effects of the disorder."

    New devices, similar to commercially-available TENS machines, could potentially be produced to be used by young people with TS to 'train' their brains to help them gain control over their tics, offering the benefit that they could be relatively cheap and could be used in the home while performing other tasks such as watching television.


    Financial, Translational, Regulatory, and Ethical Concerns for Des in ECOG-BCIS

    Translational, Regulatory, and Financial Concerns

    We expect early applications of ECoG-BCIs to leverage existing clinical devices. This has been a pathway forward for many prior medical devices. Advances in early DBS devices were based largely off of prior work in cardiac pacemaker and spinal cord stimulation devices (Coffey, 2009). We imagine a similar trajectory for DES in ECoG-BCIs. Preliminary use of DES has been enabled by investigational device exemptions (Harvey and Winstein, 2009). Further iterations of Medtronic DBS devices, such as the PC + S device, have been granted an investigational device exemption in research studies, and are improvements upon an already clinically approved device (Herron et al., 2017).

    Whenever new technology is implemented for clinical treatment, a question of cost efficacy is raised. However, we suggest that ECoG-BCIs have the potential to be cost effective long-term devices if clinical efficacy is demonstrated, as illustrated by examples such as vagus nerve stimulators and DBS. Vagus nerve stimulation for epilepsy has been show to be effective long-term, and cost benefit analysis has shown that the cost of the treatment pays off within a 2 year period (Boon et al., 1999). Although it is not universally the case, DBS in general is thought to be cost effective, when looking at studies across European and North American Centers (Pereira et al., 2007). It has been noted that during the adoption of DBS large-volume hospitals had lower prices and superior short-term outcomes, which is something to be aware of in the translation of ECoG-BCIs into the clinic (Eskandar et al., 2009).

    Ethical Concerns

    Ethical concerns are critical to address for any engineered device which is implanted in a patient. A previous review has explored some of the ethical concerns for BCIs (Klein and Ojemann, 2016), and we seek here to highlight some of the concerns which are particularly relevant to ECoG-BCIs with DES.

    Articulating the potential risks and long-term requirements for an ECoG-BCI, particularly with DES, is essential for appropriate informed consent. Biologic risks such as infection, seizures, and tissue damage from stimulation (Cogan et al., 2016) are accompanied by technological concerns such as repeated surgeries for battery replacements, heating due to potential wireless charging, and lifetime electrode wear from repeated stimulation (Klein and Ojemann, 2016).

    Privacy and security are another key aspect in implantable medical devices, particularly with any BCIs that communicate signals wirelessly or can be programed wirelessly. One can imagine situations where a stimulator could be set to either less than therapeutic levels or to unsafe levels, by malware transmitted to the ECoG-BCI device. Research efforts that build on current security and privacy protocols for medical devices are required to ensure neural signal security and protection against malevolent programing.


    Nervous System

    Patrick has been teaching AP Biology for 14 years and is the winner of multiple teaching awards.

    The nervous system is a network of neurons that send signals to different parts of an organism's body to coordinate the actions of the organisms. Most animals have two parts to their nervous systems - the central nervous system includes the brain and spinal cord while the peripheral nervous system includes sensory neurons and nerves. The nervous system is different from the endocrine system because its messages travel more quickly and don't last as long.

    One of my favorite systems to teach about is the Nervous System and this is because it's the voice talking inside your head it's what's watching me right now and the Nervous System is the one of the two major control systems of the body it works with the endocrine system to help control and regulate the activities of the body and maintain homeostasis. Now when studying the Nervous System you got to be kind of careful because it's been something that's been just inspiring scientists to dive into the research for years and years and so each scientist tries to organize it and they've organized it in many different ways and so sometimes kids get confused which ones is what? Well there's one way of organizing things based on essentially it's like Geography it's just where are they continent and that's saying the central nervous system versus the peripheral nervous system.

    The central nervous system is the brain and spinal cord alright? The stuff in the middle, whereas the peripheral nervous system is all of the nerves coming off of the brain called cranial nerves and all the nerves coming out from the spinal column the spinal cord called the spinal nerves alright? Now within the peripheral nervous system they'll make the distinction between the somatic nervous system which is the part of your nervous system that controls your skeletal muscles in other words it's my somatic nervous system that I actually or activate in order to do this or that why I don't know but autonomic nervous system controls everything else now that's a really broad category because its really a lot of things. It's the autonomic nervous system that helps you regulate how open or close blood vessels are two different parts of your body your autonomic nervous system adjust the size of the pupil the hole in your eyelids that allows more or less lighting based on how much light you're looking at.

    In general people think of this somatic nervous system as being the voluntary part the consciously controlled part while the autonomic is the unconsciously controlled stuff. Now again there's some blowing going on here, when you walk very rarely do you actively sit there and think "how I'm I balancing? How do I need to adjust the muscles of my trunk my abdomen to keep me from falling over" even though it's technically that would fall under the somatic nervous system and autonomic stuff well you can have some input into that if you start working under those Buddhist Monks who'll site there and they can learn how to control blood flow and other really bizarre things.

    Now within the autonomic nervous system there's a further subdivision, there's the sympathetic nervous division or nervous system and the parasympathetic nervous system or nervous division. Now the sympathetic division in general you can lump that together as it controls the fight or flight type responses in other words getting you ready for action whereas the parasympathetic nervous division in general gets you ready for resting and repairing now usually most body parts are being given signals by both of these and they're usually some kind of balance your very rarely all the way sympathetic and no parasympathetic or vice versa and when you're going through your normal life, there are just sitting there adjusting based on input on what your body needs and even your conscious mind can influence this.

    Now to help you think through what would the sympathetic nervous division control? What kinds of body parts would it send blood to? What kinds of actions or effects would it have on your body and versus the parasympathetic, let's start thinking about hmm close your eyes and just kind of relax a little bit and in your head imagine its 3:00 a.m. you're in your bed oh you're just sleeping you're just doing that kind of surfing between consciousness and rest and you just feel so wonderfully relaxed, the room is dark it's perfectly quiet and all of a sudden you hear 'pop' and somebody licks your ear. Now how would your body react? Your heart would start increasing as the sympathetic division says "whoa we need to run away or kill the killer clown" you would you would open up the blood vessels to the large muscles of your arms your legs getting ready to run away or engage in your Ninja battles with the killer clown. The opening of your lungs the bronchi's and bronchioles will spasm open to allow more air flow because engaging in Ninja battles with killer clown takes a lot of oxygen so you need to start to breathing faster and deeper. Now what parts of your body don't need blood at that moment well you don't need your immune system to fight off the killer clown now you may get some diseases later but right now you need to focus on fighting killer clown that's why long term stress can cause problems with your immune system.

    What else don't you need? Well you had a nice dinner few hours ago but you don't need to digest it right then so you shut off blood supply to your digestive system slow it down because you don't really need it and sometimes that's maybe why you go hmm if you've got too much food in your stomach when you all of a sudden go ah ah ah I need to fight your stomach may go, I can't handle this and reverse the pumps. Now unless you've really got a thing for killer clowns what other system don't you need at that moment? The reproductive system so the blood supply to there gets shut down and you just are ready for fighting and flighting. Now, what's an opposite kind of situation, Thanksgiving, you eat Thanksgiving dinner, you have your portion of the turkey, you have about 3 pounds of turkey, you have mashed potatoes you have everything else and then you sit on the lazy boy recliner and then your body says, we do not need to have heart-rate racing, we do not need excess air in the lungs, we do not need your muscles to be pumping and using lots of energy and instead it shuts it down. Digestive system gets a lot and everything is good.

    Weirdly enough the sympathetic division does activate one activity of the reproductive system and that's either orgasm or it can actually activate labor which is why that stereotype of the woman giving birth and when she gets trapped in the elevator there actually is some legitimate see to these this means that if a lady is walking around she is looking pretty pregnant don't just jump up behind her and go aah and attack her with her with the chains that's not just nice to do.

    Alright, now I can go through the structures of the spinal column or the spinal cord but what most people want to know about is the brain, so let's take a look at the brain. There's 4 major regions of the brain the brain stem, cerebellum, diencephalon and cerebrum. If we take a look at this diagram here, this portion here the light blue weirdly purple and light green thing there that is the brain stem. This the bottom of the brain and even though this is not quite accurate you could think of it as the part that evolved first and it deals with those basic needs this keeps your heart going your lungs breathing these are keeping you not dead kind of activities. Now there are some other things that are involved there besides just keeping you not dead there are some visually reflexes and some other things plus all the signals that are coming up the spinal column right at the bottom of this they're passing through the brain stem.

    Now this weird lump the a reddish lump that's sitting behind the brain stem it's called the cerebellum which means little brain because it actually looks a lot like the bigger cerebrum that sits on top and you can even see it has it's white matter in this thing which means white or tree of life it's got its white matter on the inside just like the cerebrum has white matter in on the inside and grey matter on the outside. What does the cerebellum do? It does a number of things but some of the most important things that it does it helps regulate and coordinate motor control. Now when you wish to move your right or left arm you don't sit there and hope that your cerebellum does it that's what the cerebrum's involved with but the cerebellum is the thing that says "I wish" no the cerebellum says "I want lift my left arm" the cerebellum says "well okay but I know Newton's third law for every reaction there's an equal on opposite reaction if I lift this arm I'm going to fall forwards" so the cerebellum says, "tighten up trunk and keep me from flapping over" when the cerebrum carries out it's action and it does that kind of smoothing things out if this is the CEO of motor control, this is the middle management that makes the CEO's directives actually becomes a reality.

    Now you may not realize how much of this actually regulates as I said it's involved a lot in balance and it helps coordinate actions and a lot times if it thinks the cerebrum's made a mistake it will override it this is why some times if you're trying to do a muscle activity like walking or climbing especially if there's something complicated if you start to think about what you're doing you may get screwed up. Now here's a weird little thing that you can do, stick out, sitting down stick out your right leg and start rotating it clockwise for you that we'd be rotating it like this then with your right hand in the air draw the number 6 what would happens to your leg? That's your cerebellum saying warning CEO stupid, stop that cerebrum and it overrides.

    Alright sitting on top of the brain stem this weirdly yellow thing here is the diencephalon and its such a little property it's so important this is where a lot of relay relying of information starts happening. This part decides where things should go in the cerebrum plus it starts doing a lot of the initial analysis of the data that's coming in and out of the brain and it starts making some decisions. This is also where a lot of autonomic control the body is decided upon. You see this little dangly guy there that's the pituitary gland the master gland of the endocrine system and it's the diencephalon that controls the pituitary gland so this is involved in a wide range of things especially with this little part here called the hypothalamus you can be involved in deciding whether or not like something it's involved in thermoregulation lots of functions are located there.

    Up here, is the cerebrum this is the perhaps most recently developed of the parts of the brain and this is what people think of as the brain. This is where your conscious thoughts probably mostly exists. Now it's divided into primarily 4 major lobes the frontal lobe in the front, the parietal lobe here, in the back you have the occipital lobe and to the side this is a kind of a view of the brain you have the temporal lobe. I often think of it kind of like a boxing glove where the thumb is the temporal lobe the fingers are the frontal lobe, the back of the palm is the parietal lobe and then it breaks down occipital lobe is the back here, weirdly enough vision analysis happens on occipital lobe I don't know why its not the front it make lot more sense. The temporal lobe which is right by the ear hey! That makes sense it's involved in the analysis of sound its also involved in analyzing things like smell, there's a number of other functions that go on in there involving there's some language stuff that goes on in there and memory is actually helped out by the temporal lobe. The parietal lobe does a lot of analysis of touch which you think of us touch and in fact right where you go from parietal lobe to frontal lobe you have this ridge called the primary somatic motor, primary somatic sensory area where you have the individual neurons that are listening to signals from different parts of your body and they've actually done things where they run along with electrodes somebody's that little ridge there and you the person will say "I'm reporting tick lings sensation or something" and it seems to run along their body and they can map it out and so you'll have lots of that brain portion dedicated to analyzing information from your hand but not so much to analyzing information from your elbow. Similarly the frontal lobe has right by that has a ridge that controls those muscles and again if you run your electrode along it you'll see the person won't feel anything but their body will start to move and that's called the primarily somatic motor area. The rest of the frontal lobe is involved in things like executive function and conscious decision making and speech so this is where you start thinking hmm what do I really want for my birthday now other parts of the brain may want may come up with I'm hungry but you may be thinking yes birthday cake is nice but I think I want a leather jacket. These portions of it right here they're involved in very long term judgment and this is the part that right now as a teenager if you're watching this, this is the part that this is fascinating to me, it's growing and developing right now which is why everyday as you age you're getting smatter and wiser and assuming that you don't do things to impede it's development, you're going to be a very wise and smart individual especially after watching this video.


    Intracortical dynamics underlying repetitive stimulation predicts changes in network connectivity

    Targeted stimulation can be used to modulate the activity of brain networks. Previously we demonstrated that direct electrical stimulation produces predictable post-stimulation changes in brain excitability. However, understanding the neural dynamics during stimulation and its relationship to post-stimulation effects is limited but critical for treatment optimization. Here, we applied 10Hz direct electrical stimulation across several cortical regions in 14 patients implanted with intracranial electrodes for seizure monitoring. The stimulation train was characterized by a consistent increase in high gamma (70-170Hz) power. Immediately post-train, low-frequency (1-8Hz) power increased, resulting in an evoked response that was highly correlated with the neural response during stimulation. Using two measures of network connectivity, cortico-cortical evoked potentials (indexing effective connectivity) and theta coherence (indexing functional connectivity), we found a stronger response to stimulation in regions that were highly connected to the stimulation site. In these regions, repeated cycles of stimulation trains and rest progressively altered the stimulation response. Finally, after just 2 minutes (10%) of repetitive stimulation, we were able to predict post-stimulation connectivity changes with high discriminability. Taken together, this work reveals a relationship between stimulation dynamics and post-stimulation connectivity changes in humans. Thus, measuring neural activity during stimulation can inform future plasticity-inducing protocols.


    Watch the video: Πώς σχηματίζονται οι αναμνήσεις και πώς τις χάνουμε - Κάθριν Γιάγκ (July 2022).


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