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It means DBS technique type of transcranial?
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No, it is the placement of electrodes in the STN.
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In a recent study published in the journal "Brain Stimulation," researchers found that transcranial direct current stimulation (TDCS) applied to the prefrontal cortex of the brain can help reduce symptoms of depression in people with mild to moderate depression. In the study, participants received TDCS for two weeks, five days a week, for 20 minutes each session. Results showed that participants who received TDCS had greater reductions in depression symptoms than participants who received a placebo.
However, other studies have shown that the effectiveness of TDCS for treating depression is limited. In a recent study published in the journal "The Lancet Psychiatry," researchers found that TDCS applied to the prefrontal cortex did not produce any difference in depression symptoms between participants who received TDCS and participants who received a placebo.
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TDCS presents both potential and limitations in treating depression. The discrepancy between the studies you cited underscores the complexity of depression treatment and the need for further research. This means that TDCS as treatment necessitates more comprehensive studies to fully understand its efficacy and role in the context of complex psychological and health factors.
The relationship between depressive symptoms, sense of self, and overall health seems to be important in this sense ( ), putatively highlighting the multifaceted nature of depression. This type of research, including the sense of self in a bigger picture, contributes to our understanding of depression's broader impacts and may inform future therapeutic approaches, potentially including TDCS.
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Greetings all, I am a fifth-year medical student, and currently trying to find a thesis topic. After medical school, I would like to pursue a career in neurosurgery, and therefore, I would preferably welcome suggestions within this discipline. I have conducted my research, and I have formulated a list of areas I would like to explore further. This includes : Implications of deep brain stimulation within neurosurgery A collaborative approach to neurosurgery involving interventional radiologists Having listed topics I am keen to conduct my thesis on, I would be grateful if anyone could suggest particular questions surrounding these. Although I gravitate toward these topics I am open to any suggestions in regard to good questions for my thesis.
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Strongly agree Professor.
Attention to this topic I think is new. What is more there also no accurate research yet about the size and impact of dynamics of cerebral venous circulation.
Let me put here a hypothetical problem:
If Hitler and Moussillni had had aplastic or hypoplastic cerebral veins causing severe IH, neurosurgeons would be able to prevent 2nd world wars.I donnot know anything about autopsies done for their brains.I am only trying to motivate you Dr Pars for this topic.
Dr Pars Professor Franz is pointing to you the point which will lead to a neurosurgical cure. I think that he spent lot of his career on this point. (Antero and retrograde interplay)
Imagine Dr Parsa you are saving many brains from dementia and many others from misdirection to psychiatric clinics.
My best wishes to you and my respect and gratitude to Professor Franz.
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There's a weird issue. I have a stim box, which has 2 entrances, one called "act.", and another one - "ref". So if I plug a bipolar electrode in it, so 1 electrode goes to "act." and another to "ref", I see bubbling on only one tip, instead of seeing it on both. If I exchange places, where electrodes connect, I see bubbling on another tip. As I know, it should not be so.
So, do you know, what's the problem here?
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Great! Happy to help.
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I am looking forward to getting a TMS unit to study the human visual cortex. In addition to a single pulse, I will routinely use cTBS. I am debating between magventure and magstim. I've used the magventure with brainsight during my postdoctoral research and am comfortable with it. But this recent Brain Stim paper (attached) biases me towards the magstim.
Any thoughts from the TMS experts on RG?
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Yes, with a brainsight neuronavigation. I am inclined towards Magventure as well!
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What are different coil shapes used in Transcranial Magnetic Stimulation? What are their differences (in induced current)? Do they have different applications?
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Hi,
Actually, the influence of inductance value in a coil on TMS is eddy current strength. In addition, the coil design in physical configuration can affect the TMS distribution or depth. The TMS coil with eight shapes is commonly used in clinical application due to better high resolution than the round coil.
You can refer to the article below. Good luck!
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I have used TNS & TMS & TACS systems which resulted in the patients awakening.TDCS was a bit effective but even this caused the patient to wake up after some time .
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Although it is difficult to stimulate a human brain while sleeping, however, it's not entirely impossible. TMS would be the best bet at a low RMT keeping the coil holder and navigation fixed beforehand. Also, tDCS can be helpful, however, due to relatively large circumference preferably use TMS.
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Quite a few published researchers are using Amrex branded sponge electrodes with banana jack connections for 1x1 low resolution tDCS. We have attempted to use them & have encountered several problems including one serious safety problem.
The electrode in question is a 3" by 3" square non-conductive rubber frame containing conductive wire mesh overlaid with a removable coarse kitchen-type sponge that protrudes out of a 2" by 2" aperture when soaked in saline. The rubber frame is stiff & does not conform well to the curvature of the cranium, especially with smaller subjects. This in turn results in difficulty placing it accurately & reproducibly & also in making good & uniform electrical contact. Though the maximum contact area of the sponge on the scalp is ideally 4 in² (25 cm²), in practice it is considerably less & variable with only a central area of contact which can be approximated as a circular disc inscribed within the 2" by 2" square aperture. This leads in turn to the most serious problem:
Injected current levels up to 2.0 mA are routine in tDCS research. The research community generally accepts a current density limit of .08 mA/cm² for the safety of the subject's skin in contact with the electrode & also to minimize potential damage to the underlying brain tissue. Even if the 2" by 2" sponge made perfect contact with the skin, at the 2.0 mA injected current level the current density limit is reached, exactly, as bulk current density = current / cross-sectional contact area = 2.0 mA / 25 cm² = .08 mA/cm². But these electrodes do not make perfect contact even when the they are secured tightly because of the rigid frames enclosing the sponges. So the contact area is rather less, resulting in the denominator being smaller and the current density necessarily exceeding the safety limit. Even at somewhat lower levels of injected current, taking the variable contact area of the sponges into account, the current density could easily exceed the safety limit. Furthermore, this is a very coarse bulk analysis. Taking nonhomogeneity, edge & corner effects into account, local areas of unacceptably high current density are unavoidable & can be demonstrated convincibly with a more sophisticated analysis (one using finite element methods for example).
Yet another practical problem with these electrodes is they have a strong & pungent odor which research subjects find objectionable, penetrates their hair & endures on the electrodes even after successive washings. If one electrode is placed supraorbitally, as is a common position in tDCS, the obnoxious smell in close proximity to the subject's nose even has the potential to affect the outcome of the experiment because it induces stress & stress-related neurological activity that has the potential to confound results.
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These areas were stimulated in mice in a work by Moshel et al (2005) and I would like to understand where the corresponding areas are exactly situated in human.
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I Agree With Guy A Orban
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In specific could stimulation of the right DLPFC have a different effect to stimulation of the left hemisphere?
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Nice Contribution Michael A. Hunter
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I am currently testing for my undergraduate dissertation looking at TDCS . I was wondering if what was done/thought/spoken about during the stimulation would change the effect of the TDCS at all?
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Good Answer Christopher S Y Benwell
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In a study looking at effects ofTDCS delivered at rest, would having a programme for the duration of stimulation (20 minutes) be a useful means of control?
Any advice or relevant literature suggestions would be greatly appreciated
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I Agree With Wei-Peng Teo
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Hello researchers,
I'm planning to apply tACS on the scalp in corrispondence of two different cortical areas by using a multi-channel device (Enobio/Starstim, neuroelectrics) . Thus, I will use three electrodes, two "active" and one "return", but I'm wondering whether the value of the current intensity might be devided between the two "active" electrodes. For example, is 2mA of amplitude splitted in 1mA for active electrode 1 and 1mA for active electrode 2.?
May you suggest any work where I could find information about this issue?
Thank you in advance for any answer you may provide.
Gabriele
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Nice Dear Gabriele Fusco
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With the 1.27mm diameter of DBS electrodes often leading to the development of scar tissue, and evidence that electrodes with diameters near the size of neurons, approximately 30 microns, are less likely to induce such scaring, can stimulating electrodes of that size or smaller be expected to perform as well as current DBS electrodes? Is there a minimum optimal diameter for neural stimulating electrodes?
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Good Answer Enrico Marani
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Dear friends
I am a PhD student and I want to design a stimulator for brain application. but I don't know how to start. I really need a good reference or someone who be a partner and help me with that. If someone is working on this subject please lets me know. I would appreciate if anybody did it for me.
Regards
Mostafa
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I try to record fEPSP in submerged patch clamp setup.
But, I can't record fEPSP in the acute slice. I really don't know the reason.
1. For recording, I use HEKA EPC 10 double.
2. All slices incubate in the slice keeping chamber for 1~1.5h at 32 Celsius in ACSF.
3. Components of intra and bath solution : 126 NaCl, 3.5 KCl, 1.25 NaH2PO4, 1.6 CaCl2, 1.2 MgSO4, 10 Glucose, 26 NaHCO3, 5 HEPES (PH= 7.3-7.4, mOsm= 300-310)
4. ACSF at 30 Celsius, perfuse rate is 2ml/min during fEPSP recording .
5. I set Current clamp mode and holding 0pA. And, I use 1~3 mohm recording electrode.
6. To record fEPSP, I tried to inject from minimum to maximum level of stimulation through simulator I have. Nevertheless, I can't detected fEPSP.
7. In addition, it was confirmed that EPSC and LTP were induced well in the same slice.
8. Before fEPSP was detected once in organotypic culture.
Each picture shows patch clamp setup about submerge state, average distance between bipolar simulator and recording electrode(100~200um), fEPSP in organotypic culture.
Questions
1. Is there anything I missed from my protocol to measure fEPSP?
2. fEPSP recorded from organotypic culture look like fIPSP. What's the reason?
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I agree with the comments regarding the filter change, electrode position, lower submerged setting. However, there is still one basic condition: careful preparation of acute slices. It looks like they're not alive.
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Hello, everyone. I am trying to find a method which can monitor temperature changes in brain caused by brain stimulation. Could you help me to find a review paper about it or send me several publications. Many thanks
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MRI thermometry is another method which provides live intracranial temperature monitoring, especially during procedures such as MRgFUS. In the case of conventional DBS leads, care must be taken to ensure the DBS systems are MRI-compatible. Tissue temperature readings immediately surrounding the electrode may be affected by the MRI procedure itself, however.
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Does Deep Brain Stimulation work on the Amygdala itself or on connection between amygdala and medial Prefrontal Cortex too?
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It is only theoretical, but practical it is not possible. Everything you read, must not be true!
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Dear Colleagues,
Perhaps you could help me find answers to several questions on the neural organization of alphabet and number recitation:
1. Could recitation of numbers and letters rely on phonological long-term memory without accessing lexical information? Alternatively, could lexical information be accessed only for numbers (since they are words) but not letters (that are not words)?
2. Several neuroimaging studies (including clinical reports) have shown a dissociation between letter and number sequencing (recitation, reading and writing). Why do you think this is the case?
3. A patient could not recite the alphabet but could sing it upon electrical brain stimulation. Any suggestions why this happened?
Help with any of the questions will be greatly appreciated!
Thank you!
Monika
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Dear Monika! Please see related articles in Attachment. All the best. Vladimir
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tDCS and tACS are forms of neurostimulation that  delivered via electrodes on the head and have therapeutic effects.
I want to know which one has a longer-lasting effect.
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Hi Fateme,
if the question stems from the need to find a suitable tES intervention, I would suggest to start with the analysis of psychopathological/neurobiological mechanism responsible for the "to-be-treated" phenomenon (i.e., is it related to a decreased activity of a brain structure/network or is it related to certain bands of oscillatory power?).
Although you could compare the duration of tDCS vs tACS aftereffects (e.g., reviewing single or multiple session tES studies), such comparison might not be therapeutically valid given that tDCS and tACS induce qualitatively diverging effect and you would need to consider WHICH of the effects are meaningful for the particular therapeutic intervention (rather than which lasts longer).
On the other hand, both tDCS and tACS are assumed to modulate neuroplasticity, so perhaps this could be set as the common feature, enabling a meaningful comparison to start with.
Best, M.
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There are a lot of invasive technologies in use today that are used to stimulate organs, the nervous system, the brain, and pain receptors in the body.
One example, would be a device that stimulates the vagus nerve, relieving arthritis pain. https://blog.applysci.com/?p=3170
Where can I source a list of the frequencies, pulse duration, and voltages used in such applications?
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It depends on the region and target for stimulation. For example, in deep brain stimulation, Subthalamic nucleus is the target for Parkinson's disease. And the standard clinical stimulation parameters are: 130 Hz, 65µs pulse width, cathodic first, rectangular pulses, usually current stimulations. The amplitude varies according to the electrode dimensions. From couple of hundred µA to tenth of mA. The reason they use current stimulation instead of voltage stimulation, is that the electrodes impedance could change over time, and in order to keep the delivered charge consistent, current stimulators are the way to go.
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Feeding knowledge directly into your brain, just like in sci-fi classic The Matrix, by a simulator which can feed information directly into a person’s brain and teach them new skills in a shorter amount of time, comparing it to “life imitating art”. I think inventing a devive that feed skills directly into a person’s brain is little far from believing . But what if build a device that stimulates some parts of a person's brain that related to the new skill that person is learning .so ,that person by using such a device could learn that new skill in very shorter time.
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People are working on to improve learning by brain stimulation. you can find several papers on brain stimulation.
As far as direct feeding is concerned, it might be possible but will take some time for science to reach there.
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In most diseases with no cure or long-term treatment, there are different shortages in the body from our brain's function to lack of Nutrients. Maybe we can stimulate particular parts of patient's brain to act differently and control the body to fight better with illness.
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Few years ago the scientists from the Department of Psychiatry Medical University of South Carolina submitted a research paper claiming a similar preposition that electromagnetic stimulation of the frontal lobe of the brain may cause to reduce weight. I received that manuscript for the review from the Medical Journal "Obesity".
My only and key question was that did the researchers take into an account the subNucleus load of the neuroinvasive viral genomes that continually proliferate which in turn. compromise the cellular homeostasis?
Obviously. the answer was no. Therefore, the editor of the journal declined its publication.
Now. EMG stimulation is very hypothetical and cant be used indiscriminately for the whole brain. All neurons not typically dealing with the uniform pathology. Different sections of the control system may be dealing with dendritic molecular change or cellular metabolic challenge or Nucleus or genetic patho-kinetics.
If the frequency of the source becomes intolerable for the brain tissue, of course it will covey more harm to the tissue than favor.
Nucleopathy is a new dimension now leading to best understand the pathophysiology of the brain.
We at the NIDS Treatment & Research Center are Launching this March a New Discipline of Medicine the NUCLEOPATHY.
This will help you understand the origination of all diseases and how to rectify them.
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Can haloperidol induced catalepsy model be used as parkinson's disease model to study Deep brain stimulation (DBS) or 6-hydroxy dopamine ( 6-OHDA)  bilateral lesioned model is more relevant? Are there any models which is better than Haloperidol induced catalepsy model or 6-OHDA model, if yes which one is it and why. Thanks in advance for kind help.
Best wishes,
Mohsin 
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Thank you very much Ali! The study seems very interesting.
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I have been doing research on this topic, but have found little empirical evidence supporting or denying its effects on brainwaves. I am currently in the process of designing experiments to see if these frequencies affect mood or have any noticeable result, but I need more resources on what has been proven or disproven about them and to what degree they are placebo.
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Timothy,
Are you familiar with the article I´ve linked below ?
Also, if you´re ever up for a "frequency ride", I´ll be glad to share some of the tools I´ve used to both tangibly affect my mood and performance and help many others do so. 
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Experience with off label deep brain stimulation in psychiatry.  
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Overall only about 200 patients have been treated worldwide, all with severe forms of TRD. This means that they did not respond to psychotherapy, pharmacotherapy and in most cases ECT. I am not aware of a single case of a patient treated with DBS who is not pharmacotherapy resistant. The overall efficacy has not been established yet. Please keep in mind that stereotactic neurosurgery is invasive and carries a 0.5-1% risk of hemorrhage.
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Is there a way of single pulse electrical stimulation through DBS electrodes after they have already attached to the pulse generator? or, the only way is to stimulate through the externalized electrode immediately after surgical operation in the period before the electrode will get attached to the pulse generator? are there any pulse generators capable of doing single pulse? Medtronic ones are able to produce 3Hz stimulation as the lowest stimulation frequency. 
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Yes, currently we can lower stimulation frequency only to 3hz with internalized DBS. We used peritriggering technique with 3Hz DBS to couple motor cortical TMS to induce plasticity (Udupa et al, 2016 JNs). As you suggested with externalized electrode we can stimulate at any parameters as required. However, newer electrodes with special programming parameters are coming out which should deliver single pulses. 
Udupa K, Bahl N, Ni Z, Gunraj C, Mazzella F, Moro E, Hodaie M, Lozano AM, Lang AE, Chen R. Cortical Plasticity Induction by Pairing Subthalamic Nucleus Deep-Brain Stimulation and Primary Motor Cortical Transcranial Magnetic Stimulation in Parkinson's Disease. J Neurosci. 2016 Jan 13;36(2):396-404. doi: 10.1523/JNEUROSCI.2499-15.2016. PMID: 26758832
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Hi , As we know the bioelectric scientists can  stimulate different kinds of senses like  perception   and vision in patients and also can eliminate  senses such as pain and pruritus.
Now my question is: does it possible for scientists to make stimulations in CNS of patients with nightmares in order to cure their nightmare and making   desired  dreams?
thanks for you attention,
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The following articles may have relevant literature, but I don't believe the field has reached that stage:
Investigation of dream reports after transcranial direct current stimulation (tDCs) during slow wave sleep (SWS).
By Jakobson, Antonia J.; Fitzgerald, Paul B; Conduit, Russell
Sleep and Biological Rhythms, Vol 10(3), Jul 2012, 169-178.
Despite being a prominent feature of REM sleep, dreams have also been reported from NREM sleep. Neuroimaging studies have revealed regional patterns of brain activation and deactivation during REM and NREM sleep, with frontal and posterior parietal cortices implicated as brain regions involved in dreaming. From our recent stage 2 study it was revealed that tDCs of these brain regions during this stage of sleep resulted in an increase in reported dream imagery. Thus, the aim of this study was to investigate the effect of simultaneous anodal and cathodal tDCs applied to the right posterior parietal and frontal cortex (respectively) during SWS on dream recall. After 60 s of continuous SWS, participants were administered either tDCs, low tDCs, or blank control, followed by a 60 s delay period to confirm SWS before waking the participant for dream report collection. These conditions were administered in a counterbalanced order across the night. Analyses revealed no significant difference between conditions in the three dream measures. However, an analysis of visualizable nouns to total words revealed a significantly higher ratio in the low tDCs condition compared to the tDCs condition. It was concluded that tDCs had no appreciable effect on reported dream imagery. However, such findings are preliminary as they are from a research protocol which is in the process of refinement with more definitive results expected in future. Thus, further studies should now investigate the application of tDCs using improved methodologies and to other cortical regions implicated in the process of dreaming. (PsycINFO Database Record (c) 2016 APA, all rights reserved)
Treatment with AC pulsed electromagnetic fields induces vivid colored dreams in multiple sclerosis.
By Sandyk, Reuven
International Journal of Neuroscience, Vol 96(1-2), Oct 1998, 45-52.
Describes the cases of 2 women, aged 33 and 41 yrs, with multiple sclerosis (MS) in whom transcranial alternating current pulsed applications of electromagnetic fields of 7.5 picotesla flux density restored dream recall and induced 4 to 5 mo later vivid colored dreams typically associated with REM sleep. Melatonin (MT) has been reported to increase the amount and duration of REM sleep, decrease REM sleep latency, and additionally induce vivid colored dreams in normal Ss and narcoleptic patients (e.g., M. Mirmiran and P. Pevet, 1986). Since nocturnal MT secretion is diminished in MS patients who also demonstrate a high incidence of calcification of the pineal gland (R. Sandyk and G. I. Awerbuch, 1991, 1992, 1993), it may partly explain why the disease is associated with disruption of the dream process and/or its recall, and also with loss of colored dream imagery. Therefore, it is possible that in these patients, the experience of vivid colored dreams during the course of magnetic therapy, which affects MT production, was related, at least in part, to enhanced nocturnal MT secretion. The recurrence of colored dreams coincided with a period of distinctive improvement in visual symptoms, suggesting a relationship between colored dream experiences and visual symptom improvement in MS. (PsycINFO Database Record (c) 2016 APA, all rights reserved)
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I am trying to investigate learning and memory consolidation over sleep/wake using brain stimulation. Multiple studies have used the paired-association list learning task in the context of sleep; however, only one study has used tDCS and Sleep with this paradigm. Unfortunately, this study made use of German words. Can someone recommend an English database for me to design this experiment?
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Depending on what variables you want to control (word frequency, part of speech, number of letters, etc.), you might try any of the following:
MRC Psycholinguistic Database (http://www.psych.rl.ac.uk/)
University of South Florida Free Association Norms (http://w3.usf.edu/FreeAssociation/)
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What is the best book on the brain waves?
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BLUME'S ATLAS OF EEG
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Dear tACS community, dear physicists and electrical engineers
I would be very grateful if somebody with the appropriate training could please clarify how to calculate the current density under the stimulation electrode for an alternating current? Based on the standard set by tDCS research (direct current stimulation), some researchers variably divide either the half peak maximum amplitude or the peak-to-peak amplitude by the electrode area, while others say that this measure is inappropriate for AC currents. What is the correct measure that relates injected current and electrode surface area?
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With AC currents, current density depends on the frequency: for low frequencies you may calculate current density similar to DC.
For higher frequencies, the skin effect cannot be neglected.
Regards
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Like most researchers in the tDCS community, I'm looking to induce persistent LTP-like effects.
The current literature is informative insofar as highlighting that multiple sessions of tDCS appear to enhance the strength and prolong the duration of resulting after-effects. The time at which repeat stimulation is administered also appears to be crucial but as yet there is little-to-no consensus on the most optimal parameters to use, including appropriate inter-stimulation-intervals. More recently, there seems to be a suggestion that implementing within-session intervals instead of continuous stimulation could be the way to go, however, the related studies only cover single sessions and don't comment on the frequency at which subsequent sessions of stimulation should be delivered.
Does anyone have any experience of attempting to induce longer lasting modulations - successful or otherwise? I'd appreciate advice on what to trial, what to avoid and whether you've noted differences between target populations (healthy/clinical, young/old etc) with regard to the parameters that show the most potential.
Thanks in advance!
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Hello Claire, 
    I think you mentioned a very important issue, referring to the practice of precision medicine, which needs to be considered individually.
    Our ongoing tDCS study includes 12 times treatment, 3 times for a week. Some people like Monday+Tuesday+Wednesday, some prefer Monday+Wednesday+Friday. Frankly speaking, the inter-stimulation intervals are scheduled by the participants.
    While, whether the tDCS treatment has the feature of "dosage-dependent"? If so, how to define the "dosage"? The current wrote in proposal is not the best candidate for "dosage". Because the current (2000 mA) set by tDCS machine is not the same as the one "arrive at" the cortices.
    Thus, before finding the optical intervals, we still have a lot of work to do. :) 
    Best regards and good luck,
    Hanna
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Hello,
 I  was looking for some tDCS stimulation software and fortunately found COMETS (http://cone.hanyang.ac.kr/BioEST/Kor/Comets.html) . I would like to dig bit deep into it and started to examine the output file POTENT.OUT and other files. Could someone please help me with the following questions.
1)      The file POTENT.OUT has voxels and associated with a number, I am presuming that value as current. Am I correct here or is it Electric field, if so what are the units for that value?
2)      I happen to open POTENT.OUT file in Notepad and found 13,194 voxels and with corresponding current in each of them( example  1   0.00003467) which has 3D co-ordinates associated with those 13,194 voxels in xyz.dat file. The problem I am facing is , I couldn’t find out the boundaries associated with these voxels, like voxel number 1-1000 belong to frontal lobe, 10000-5000 belong to Parietal Lobe etc.
3)      I used MESH VIEWER to view .PLY files, the only thing I can see is brain model  but not the stimulated region in it.
4)      I would like to build my own head models, so all I need to do is get fMRI Images and get them into CURRY 7 and create boundary conditions. Is that all I need to do or any other software I need to use other than this?
 Any help is very much appreciated.
Many thanks in advance.
Regards,
Sri.
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Hi - I was just about to recommend simnibs, but I see Mohsen has beaten me to it! If you do use it, pay close attention to the recommended MR sequences that the authors suggest are optimal for segmentation. These are described in more detail in
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Hi,
I have a budget of ~20.000$ and I would like to buy a system to record and stimulate (electrical micro-stimulation) from laminar electrode (i.e. Plexon U-probe http://www.plexon.com/products/plexon-u-probe). I am working with behaving macaques. At the moment I am not interested in a perfect single-neuron spike-shape isolation. 
I would be very grateful if you could suggest me any item/company.
Thank you!
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Thank you Michael, this is a great advice!
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I am currently interested in a research on the application of deep brain stimulation (DBS) of the nucleus basalis of Meynert (NBM) for patients with dementia. Several studies in animal confirmed that the effect of low frequency stimulation (LFS) of cholinergic neurons in the NBM is able to induce cortical cholinergic release, which results functionally to cognitive improvement (Kurosawa et al, 1989). Human studies have also found cognitive improvement to some extent by LFS of the NBM (See studies by Freund et al, 2009 and Kuhn et al, 2015). Given the recent finding that the DBS mechanism of action is not merely about high frequency stimulation (HFS) inhibits neurons and LDS excites neurons (in fact, both stimulation settings excite neurons, for rev. see Montgomery, 2010), what would be an explanation that different setting of frequency parameter results in different result of acetylcholine release in the cortex?  
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Kurosawa et al (1989) used 50Hz trains. That is not low frequency, it is a normal protocol. The usual range for microstimulation tends to be 30-100Hz trains of various (short) lengths
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I use a saline solution tank and try to apply currents through electrodes in it. My problem is that the properties of the saline solution change with current passing through it and I have to re-prepare the solution. Is there a way around this?
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It's the other way around 14 cup of distilled water vs only one cup of sea water. Thank you for pointing out this mistake. Any way I repeated the experiment with distilled water and salt and a lower current and got reasonable results for various electrode types.
In a paper 
They took gray matter conductivity to be 0.33. That's why 5/15=0.33 (14 dist.wat+1 sea water)
The salt to be added to one litre of distilled water to get 0.333 S/m conductivity is from here: Figure 3 in:
I am very well aware of the 0.9% matter but I have some personal family reasons that makes it difficult to go to college for experiments.. so I am trying to make use of this time by experimenting at home
Any way for now, thank God and thanks to colleagues advice, I have some reasonable results for a start.
Having to work with applied mathematics is a bit distracting as you work in different fields ..never get time to be an expert in any single field 
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Is there any reliable study about long-term outcomes in young patients (25-35aa) with essential tremor treated with unilateral thalamic lesions or deep brain stimulation? My question is not only about long term tremor and quality of life rating scales but especially about long term cognitive impairment if any.
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I do not think is that common to have a 25-35 years ET patients undergoing functional surgery for many reasons, tremor usually become disabling and cannot be treated with meds in older patients. Shaking patients requiring surgery in that age may not have ET. Anyway, to my knolewdge VIM DBS (expecially unilateral) is quite safe as for cognition, that's why it can be done also in elderly
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Is there any research work about this subject?
Thank you very much!
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Dear Zhang,
There are a lot of side effects. Such as for example:
Suicide, worsening of mobility, motor fluctuations, dyskinesia, psychosis or hallucinations, anxiety, impulse control disorder, depression, cardiac disorder, injury, respiratory or thoracic disorder..
Some can also be associated with surgry or device: 
Impaired wound healing, intracerebral abscess or edema, dislocation of device, reoperation necessary..
Dysphonia should not be overlooked, especially in the STN DBS im.plications.
If you want to see this article:
Matias CM1, Mehanna R, Cooper SE, Amit A, Lempka SF, Silva D, Carlotti CG Jr, Butler RS, Machado AG. Correlation among anatomic landmarks, location of subthalamic deep brain stimulation electrodes, stimulation parameters, and side effects during programming monopolar review. Neurosurgery. 2015 Mar;11 Suppl 2:99-108; discussion 108-9. doi: 10.1227/NEU.0000000000000645.
Best Regards,
Dr Mehmet
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Transcranial Magnetic Stimulation has brought a lot of hope in the field of non-invasive treatment of Neurological disorders.
As it has picked my interest in the case of Parkinson's Disease, I can't help but wonder how we hope such a specific effect of TMS on PD's motor symptoms. Indeed the basal ganglia circuits is a very complex one and each structure will affect several others in an activating or inhibiting way. So how can we really hope for a specific effect, when we are merely activating a superficial region (that will of course, in turn, activate others, but still, how specific can such an intervention be) ?
There has been some effect I have seen, but, as of now (and I know it is still a young field of investigation), results are mitigated (see Benninger and Hallet review in NeuroRehabilitation, 2015 for a recent comparison of results)
Or maybe will it be more useful in combination with medication ?
Any thoughts ?
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Hi all,  
Just to add to the discussion, there has been some fairly recent work using intracellular recording [1] and optogenetics [2] that strongly suggests that one of the main targets of STN DBS is antidromic activation of cortical neurons projecting to STN . So it is highly possible that motor cortical TMS will activate these neurons orthodromically. The problem is that TMS is unlikely to be selective for one specific type of neuron and the mixed effect of activating these projection neurons, as well as those projecting to both direct and indirect pathway neurons in striatum is unlikely to be collectively helpful. It is possible that appropriate stimulation patterns could induce plasticity at the level of corticostriatal synapses, that may lead to a greater activation of direct pathway neurons, for example, and relieve some of the akinesia, but this stimulation is likely to require concomitant phasic dopamine release [3]. It is possible that strong cortical activation could lead to phasic stratal dopamine release, either by local effects within the striatum driven by strong coordinated activation of glutamatergic inputs to, say, cholinergics [4,5], or possibly by multi synaptic effects between cortex and SN/VTA. But this requires that there is sufficient residual dopamine in still surviving terminals. This would need to be proven using electrochemistry/ human studies using raclopride binding. 
Again we are back to the issue that we don't understand which cortical elements (neurons and/or glia, although the effects I speak of above are all neuronal) are directly activated by rTMS and where any plasticity that results is induced. 
Good discussion!
Thanks Aurélie,
Regards
John
References:
[1] Cortical effects of subthalamic stimulation correlate with behavioral recovery from dopamine antagonist induced akinesia. Dejean C, Hyland B, Arbuthnott G. Cereb Cortex. 2009 May;19(5):1055-63.
[2] Optical deconstruction of parkinsonian neural circuitry. Gradinaru V, Mogri M, Thompson KR, Henderson JM, Deisseroth K. Science. 2009 Apr 17;324(5925):354-9. 
[3] A cellular mechanism of reward-related learning. Reynolds JN, Hyland BI, Wickens JR. Nature. 2001 Sep 6;413(6851):67-70.
[4] Striatal Dopamine Release Is Triggered by Synchronized Activity in Cholinergic Interneurons. Threlfell, S., Lalic, T., Platt, N.J., Jennings, K.A., Deisseroth, K., & Cragg, S.J. Neuron  75: 58-64 (2012).
[5] Modulation of an afterhyperpolarization by the substantia nigra induces pauses in the tonic firing of striatal cholinergic interneurons. Reynolds, J.N.J., Hyland, B.I., & Wickens, J.R. Journal of Neuroscience  24: 9870-7 (2004).
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I want to do fEPSP recordings on the Shaffer-CA1 pathway in vivo in the middle part of hippocampus in rat. I checked the literature and found conflicting results.
For example, in the work of Doyle et al. (J Neurosci, 1996,  vol 16, 418-424) and their later works, the recording electrode was placed closer to the Bregma than the stimulating electrode was (recording electrode: AP -3.0, ML 2.0; stimulating electrode: AP -4, ML 3). 
However, in some other works, e.g., Bliss et al. (J Physiol, 1983, 341, pp617-26), it is the stimulating electrode that is closer to the Bregma  (stimulating: AP -3.4, ML 3.2; recording: -4.4, ML 3.0). Both claimed that they were stimulating and recording the CA3-to-CA1 pathway. How could they had the exact opposite way of placing the stimulating and recording electrodes when both claimed to stimulate & recording the same pathway? These  are just some examples. I found more reports with  conflicting coordinates.
I am wondering if anyone has a clearer answer on that, and can tell me the accurate way to place the electrodes on CA1 pathway in rat hippocampus.
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I want to solve your problem by presenting amazing article, which was very helpful for me when i had the same problem few months ago !!! in this article ,you will find out the exact way to locate electrodes .
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My area of research is effect tDCS (Trans-Cranial Direct Current Stimulation) on brain potentials.
I don’t have a good knowledge in tDCS modelling but would like use it a bit in my thesis. As I have already completed 2 years of my PHD I don’t want drift into new field or code the stuff for modelling. I would like to observe how current flows into brain when tDCS is applied. I looked for tDCS modelling software and couldn’t find many in my search. I found one named SPHERES (http://neuralengr.com/spheres/?page_id=17), which doesn’t have human brain model instead have a sphere but can play with parameters (amount of current, electrodes location where tDCS is applied etc).
Could anyone please help me with a simulation software where I can play with parameters like amount of current, electrodes location where tDCS is applied etc. Any help would be really appreciated.
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You can try  SCIRun 5.0  Brain Stimulator FEM Toolkit developed at the University of Utah:
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I am specifically looking for advise concerning the type of stimulator that can be used in rodents. Would it be feasible to build our own stimulator, if yes, which technical aspects should be considered.
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We use STG4008 (multi channel systems).
It is easily interface-able with MATLAB or C++. You can download any waveform into the stimulator and  trigger an output at specific time points. It is really flexible functionally and sufficiently current controlled. 
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I'm currently doing BDA (biotinylated dextran amine) injections into the motor cortex for anterograde axonal tracing. My BDA is tagged with Alexa 488 and Alexa 564. The biggest issue I'm having at the moment is that my BDA is staining the pia mater of my brain and appears to be going everywhere! I think it's contributing to some of the vessel staining I'm seeing as well. 
I've tried varying speeds and amounts of injected BDA. Pulling the needle out slowly, but none of this seems to be really reducing the spillage. 
I've attached a picture so you can see the staining all along the edge of the brain. 
Has anyone who has done this procedure before encountered this problem?
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Are you pressure injecting or iontophoretically injecting BDA?  If the former, what is the volume you are injecting?  It is possible that there will be tracer leakage out of the penetration and around the skull a little time post-surgery considering you are injecting a cortical, or superficial structure.   I have seen similar cases with 'autofluorescence' of pia mater only when I pressure inject FR and a number of AAVs.
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I'm planning to join a research group that involves Deep Brain Stimulation. So I would like to know how much of MATLAB programming I need to know in order to do any sort of signal analysis that involves Deep brain stimulation. I know the basics of MATLAB as of now. Do I need to certain methods in MATLAB in order to carry out the signal analysis in MATLAB ?
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You need to familiarise yourself with all the signal processing component of matlab. A course in signal processing with quality matlab laboratory component should help.
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Good morning, I’m doing in vivo electrophysiology in anesthetized mice. I’m recording evoked filed excitatory post synaptic potentials (fEPSP) in the hippocampus CA1 stratum radiatum after the electrical stimulation of ipsilateral CA3 axons. I would like to test other concentric bipolar stimulation electrodes but I don’t have the knowledge necessary to wisely choose a configuration that might fit my needs. Thereby I would like to learn how to choose an electrode (even another that bipolar if it is the case) that might adapt the best for the brain region on which I'm currently experimenting on (which currently is the hippocampus) and perhaps others in a near future. Thank you.
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Dear Jose,
The majority of the commercially available bipolar concentric electrodes are designed to provide the best performance in terms of spatial charge distribution. I usually work with electrodes from FHC (http://www.fh-co.com/products/research-electrodes/concentric-bipolar-microelectrodes#research-electrodes), and I can tell that they all work very well. I would specially recommend those with a beveled or pencil point shape and outer diameter ≤200 µm to reduce the tissue damage, specially when you target CA3 (~2500 µm depth in mice).
Best,
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In an episodic memory consolidation experiment there are at least three stages: 1) encoding, 2) reactivation, 3) recall. We want to see how the stimulation during reactivation stage impair memory traces. Is it necessary to ensure that the subject has done a good encoding (accuracy>90%), for example with an "old/new test" after encoding stage? I think this test could affect the results because it's a sort of reactivation.
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Any sort of test of encoding success will cause reactivation, and reconsolidation/retrieval based forgetting. Consequently, the (later) stimulation would be greatly affected by such things. Therefore your problem is understandable. 
My suggestion would be to ensure first that encoding works like you want to. Pilot the encoding on several subjects with different item and inter-item duration etc., (or other parameters) to optimize your encoding experiment, such that a sig number of subjects do well above chance; or more like 60%-80% recall. If subjects are performing too well, you make it strict. If its too hard, you make it easier, until you optimize it for a good number of subjects. 
With the assumption that this encoding experiment worked well during your piloting, you can then proceed with the rest of your experiment without having to test for encoding accuracy. 
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Electroconvulsive and electromagnetic stimulation are two therapies used in patients with depressive disorder, schizophrenia, mania and others psychiatric problems. Generally, these therapies are employed in patients who didn't have  success with psychotropic drugs. The brain chemistry is complex, but some drugs influence the neurotransmitters (dopamine, levodopa, ...). How do physical therapies affect the brain biochemistry? Can anyone indicate some book or paper about subject? I think to develop sensors for diagnosis in this area, but I don't know very much about psychiatric therapies. I would like to study more specifically this problem that affect many people in world.
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ECT is maybe simmilar with reset on computers... Very effective by catatonie and deep depression, but realy a shock for brain and body. Disbalance in neurtransmiters is not a cause of neuropsychiatric disorders - it is a consequence of different causes. Simillar as inflammation as consequence of many chemical, physical and biological pathogenic agents.
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It’s been known for decades that electrical stimulation of brain increase the extracellular concentration of dopamine significantly and helps to restore some function of the brain specially in movement disorders like Parkinson disease, dystonia etc. Recent past has also revealed that electrical stimulation of the brodmann area 25 or subgenual cingulate in human cortex help in reducing the depression like symptoms in patient suffering from major depressive disorder. Is their information available about the functional mechanism behind the induction of the dopamine and serotonin release by electrical stimulation of the brain? And, is it works for both dopamine and serotonin release differently or it works on the same principle for both? Also is this process of electrical stimulation help or induce the synthesis of the dopamine and serotonin or it just help in release of available neurotransmitters only? If later is the case what’s the intracellular concentration of the dopamine and serotonin after stimulation? I am trying to find out the mechanism about how cells maintains its equilibrium after stimulation which can increase the extracellular concentration of these neurotransmitters significantly in very short span of time and not warranting the long term integrity of cells. Any suggestion or comments would be highly appreciated.
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At least in the case of Deep Brain Stimulation (DBS), the axonal pre-synaptic terminal has the lowest threshold to activation and consequently can drive synaptic release of neurotransmitters. However, it is important to realize that the same action potential in the presynaptic terminal that causes the release of neurotransmitters simultaneously is antidrormically conducted to the cell body from which the axon arose. Further, the antidromic potential also can branch to an axon collateral in an orthodromic manner. Hence, the effects of electrical stimulation are propagated widely. Thus, it would be a mistake to interpret the effects of brain stimulation as in the case of DBS, to the structure in which the electrical contacts are located. Indeed, there is evidence the therapeutic effects of DBS in the subthalamic nucleus (STN) has little to do with stimulation of neurons in the STN but rather stimulation of the axons passing to or through the STN. It also is important to recognize that information in the brain is processed and transmitted electrically. Thus, it is the pattern of electrical activity that determines function. To focus on neurotransmitters is like focusing on electrons in a computer. Certainly a computer cannot function without electrons but there is nothing inherent in an electron that determines the functions of the computer.
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To find an alternate for brain's frequency following response
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Brain wave entrainment and modulation
can be achieved using forms of transcranial electrical stimulation, deep brain stimulation, light stimulation,, and other. Inputs. depending on brain. state.
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Which is responsible for memory saving mechanism: Neural network of brain or molecular quantum transition in definite locations in brain or selective chemical reactions all over the brain or none of them? How and where does the brain store such a tremendous amount of data? What are read and write mechanism of this data? Is the chemical -base processing dominant or physical -base one?
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The EU has decided to give a massive amount of funding for the Human Brain Project with various sub-projects, see https://www.humanbrainproject.eu for the project.
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I know UPDRS is the standard rating for clinical follow up. I am interested in any knowledge about imaging data or other means to quantify disease progression that is independant of clinical evaluation.
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Rosi - I think most clinicians are sill wedded to the dopamine story if only because it's an easy explanation for patients. Research has long switched to protein misfolding as the source of all the NDDs and conformational diseases in general. The relative failure, however, of drugs developed to reduce beta amyloid protein tangles to produce any lasting benefit to AD patients has damaged confidence in the (unwarranted) assumption that because all the NDDs are associated with protein tangles then their must be a causative connection. Research continues of course, but more circumspectly than before. There is an excellent review (BBA_Molecular_Basis_Diseases_1822_261.pdf) edited by Vladimir Uversky, that pulls it all together.
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Could transcranial magnetic stimulation (TMS) be used to create a new definition if someone is dead or not? And could it play a role in resuscitation (eg. used in conjunction with CPR for a victim of drowning).
It appears our definition of what is dead needs to be redefined. Increased number of victims of drowning, cardiac arrest etc. are being resuscitated after the normal vital signs have gone. In 2011, the medical journal Resuscitation reported the case of a Japanese woman being resuscitated over four hours after being found dead. She later went on to bear children as normal.
Those that have recovered from being "dead" for long times are often able to recount experiences of feeling still conscious while they were medically "dead."
It seems to me that we need a new definition of what dead is. I am thinking that TMS could be used to test if body parts still respond to TMS brain stimulation of a "dead" body. If there is still muscle movement, then it means electrical pathways are still intact and therefore there could be a chance for resuscitation.
I hypothesize that TMS could be used in conjunction with CPR and might help to stimulate resuscitation. Has this idea been considered and has any research carried out?
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Well, your question actually has two parts, which I would summarize as: i) could we use TMS as a tool to assess brain death and ii) could we use it to resuscitate people (in the same way cardiac electric shocks are used as I understand)?
i) Probably, yes.
ii) Definitely not.
Let’s be a bit more constructive. But first, let’s consider what TMS technique we would be speaking of. Indeed, I don’t think that TMS of primary motor cortex in order to detect movement is an effective way, for several reasons. First, you might not know the past medical history of the patient, who might have had previous brain injuries. We know that severely brain injured patients have higher motor threshold and lower responses to TMS as compared to healthy subjects (e.g. see Lapitskaya et al. 2013). Second, the current event may prevent you from noticing any limbs movement at all (traumatic lesion, physical restrains …). Finally, you will only test for a very limited amount of cerebral cortex. You wouldn’t say that complete locked-in patients are dead would you? Well, primary motor TMS wouldn’t result in any movement.
So, you may want to use the combination of TMS with EEG. That way, you can interrogate much more of the cerebral cortex, and seek a local response. While I don’t know any study on TMS/eeg in brain dead people, the EEG response should be flat. That means, no response at all. We already know what to expect from acute and chronic severely brain injured patients (e.g. see Rosanova et al., Brain, 2012), and from healthy subject during general anaesthesia (see Ferrareli 2010) and sleep (see Massimini, 2005). So this could be an effective way to detect brain capacity for consciousness in patients who otherwise show no signs of life at all. But this also has several limitations. One of them is the availability of the equipment. Second is the time require for the set-up (TMS compatible EEG requires really really good impedances, so you might count at least half an hour for a team to fix the cap). Third is that you may not have your answer straight away, as the response can be somewhat subtle. Finally, we don’t know how prolonged cold or other condition would affect the response. So possible yes, but complicated.
For the second part of your question, the answer is definitely no. Indeed, TMS works by depolarizing a group of bent axons, leading them to discharge. That response then propagates to the rest of the cortex and sometimes (in the case of motor stimulation) to the spinal cord. But, as you know, cells don’t like death. They tend to die when that occurs. Especially neurons, which can only survive cardiac arrest for a couple of minutes. When they stop working, they stop making ATP (energy). Without ATP, the membranes pumps and some of the ions channels stop working. And the differential of potential disappears with the ions balance restored. And without a membrane potential, you cannot force bent axons to discharge. So, stimulating a dead brain won’t result in any sort of reaction. Even if the brain is only dying, not dead yet, I don’t see how stimulation parts of the brain would results in restoring life. What portion of the brain would you stimulate to achieve that? Cardiac shocks only works in restoring effective rhythm when in fibrillation, meaning firing anarchically. When the heart is stopped, asystolic, electric shocks wouldn't work either. Plus, cardiomyocytes have a far better resistance to ischemia than neurons (in the order of tens of minutes).
Hopes that helps, and sorry for the rather long answer.
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For example: different people may have a different skin conductance and resistance. It may also not be possible to control the exact amount of saline. Are these differences important or not?
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With due respect Stavros, I think the problem is actually that the current delivered from the stimulator may be constant. However, most of the current is just shunted through the scalp and doesn't reach the cortex. How to ensure that the cortical current is the same is to my mind not possible at the moment.
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This is related with dopamine innervation. I want to know if it is possible to relate dopaminergic innervation of basal ganglia and sensory motor cortex for arm movements to gait.
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There are several gaits including normal walk and running. Even normal walk can be almost automatic (when you are strolling in a street) or pure voluntary (when you walk on a difficult area)
The circuit of the so called automatic gait includes basal ganglia, whilst the ¨voluntary gait¨ probably is much more cortical
This explains why patients with Parkinson disease (PD) have progressive problems with ¨automatic gait¨ but voluntary gait is normally preserved. In addition, some young PD patients may have freezing of gait...but can run without problem...or can move on four limbs...
This suggest that there are several distinct circuits for human propulsion
Gait is still a mystery
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It is difficult to generate clean clear crisp images that allow you to visualize DBS stimulating leads and local anatomy, while still staying within the Medtronic/FDA recomended average head coil SARs levels of .1W/Kg.
We are pleased with our pre-surgical targeting sequences, but are having a difficult time modifying the same parameters for post op post implant imaging.
Using a GE 1.5T with Send/Recieve head coil.
FlipAngle TE TR TI SlTh SlSep Nex Bandwidth FOV
Saggital MPRAGE 20 min full 2 0 1 15.63KHz
Axial Oblique T2 N/A 68 2500 2 0 4 15.63KHz 28
Axial T2 Straight N/A 68 5184 2 0 2 20.83KHz 28
Coronal T2 Straight N/A 68 3534 2 0 2 16.67KHz 28
Axial 3D SPGR 30 min full 2 0 1 15.63KHz 26
Axial STIR 40 3000 200 4 Intrlv 3 31.25KHz 26
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From Journal of Neurosurgery Vol 117 - No. 1 - page 370-387.
MRI Protocol for GE Horizon for lead visualization...
Scanner - General Electric Horizon
T2-weighted FSE
  TR (msec) 3000
 TEeff (msec) 87
 matrix 384 − 256
 NEX 4
 slice thickness (mm) 2.0
 interleaved imaging
 time (min:sec) 10:48
volumetric gradient echo
  type of acquisition SPGR
 TR (msec) 36
 TE (msec) 8.0
 matrix 256 × 192
flip angle (°) 35
bandwidth (kHz) 15.6
NEX 0.75
slice thickness (mm) 1.5
imaging time (min:sec) 11:00
The above protocols were used to directly visualize DBS lead placement in 44 patients. The lead placement was very clear on the presented images. If you are still having problems getting the SAR threshold down to 0.1 W/kg. You have two parameters that you can manipulate, TR and Flip Angle. In the case of the FSE, Flip Angle is not manipulable since the refocusing pulses are fixed. You can reduce the number of refocusing pulses with a lengthening of the sequence in time.
In the case of the SPRG, you can reduce Flip Angle linearly to reduce SAR, in addtion to setting a longer TR. In both cases, longer scan times are the result but that is a small price to pay for safe scans for this type of information.
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What are the standard frequency parameters for controlling tremor in Essential Tremor individuals implanted in the VIM? Is it the same high frequency centered around 185Hz, or has good control been obtained with lower frequencies?
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Ggenerally, high-frequency DBS with 130Hz is applied. Higher frequencies are considered if standard parameters do not result in sufficient therapeutic width. At first amplitude and/or pulse width are consecutively increased. Additional frequency increases can be considered as a further programming option as well as stimulation on seperate independent contacts with double-monopolar, double-bipolar or 'interleaved' programming. Best, Daniel