tag:blogger.com,1999:blog-742801720200550592024-03-21T00:31:06.304-07:004th International Conference on Neurology & Health Care<b>Theme:</b> Panoramic view of Neurology and Health Care<br>
<b>Date:</b> June 24-25, 2019 <br>
<b>Conference Venue:</b> Rome, Italy
pulsus conferenceshttp://www.blogger.com/profile/10796891539023352265noreply@blogger.comBlogger45125tag:blogger.com,1999:blog-74280172020055059.post-3304591886606441312019-03-14T06:10:00.003-07:002019-03-14T06:10:43.450-07:00<div dir="ltr" style="text-align: left;" trbidi="on">
Neurology 2019 is a grand event which is focused on the theme “Panoramic
view of Neurology and Healthcare” and ensures better advancements in
healthcare for the future.<br /> Have a look at<b><span style="color: red;"> <a data-ft="{"tn":"-U"}" data-lynx-mode="asynclazy" data-lynx-uri="https://l.facebook.com/l.php?u=https%3A%2F%2Fneurology.cmesociety.com%2Fvenue-hospitality%3Ffbclid%3DIwAR3qe2CYJ2sgyvaok6V1PowPwvTgEXhjHPok4gXJnVSuoScI1zuVqw9wBKg&h=AT3zZXEIt6PBtgnsOgm9Bco_37EA62KC0J0LV9vmUGH_GlswWSp9Bj4uvroHi-OnT-UViyajm907L_GPexbA9XO2gypwDtR8Vg7ptaWmaMpPDEWYP-Tb0AGJcdGSi6ai0TjHUyhVecuw6qXxa5zsiMpa" href="https://neurology.cmesociety.com/venue-hospitality?fbclid=IwAR3qe2CYJ2sgyvaok6V1PowPwvTgEXhjHPok4gXJnVSuoScI1zuVqw9wBKg" rel="noopener nofollow" target="_blank">https://neurology.cmesociety.com/venue-hospitality</a></span></b><br /> <a class="_58cn" data-ft="{"type":104,"tn":"*N"}" href="https://www.facebook.com/hashtag/neurology?source=feed_text&epa=HASHTAG"><span class="_5afx"><span aria-label="hashtag" class="_58cl _5afz">#</span><span class="_58cm">neurology</span></span></a> <a class="_58cn" data-ft="{"type":104,"tn":"*N"}" href="https://www.facebook.com/hashtag/neurology2019?source=feed_text&epa=HASHTAG"><span class="_5afx"><span aria-label="hashtag" class="_58cl _5afz">#</span><span class="_58cm">neurology</span></span><span class="_5afx"><span class="_58cm"></span></span></a><a class="_58cn" data-ft="{"type":104,"tn":"*N"}" href="https://www.facebook.com/hashtag/neurology2019?source=feed_text&epa=HASHTAG"><span class="_5afx"><span class="_58cm">2019</span></span></a> <a class="_58cn" data-ft="{"type":104,"tn":"*N"}" href="https://www.facebook.com/hashtag/neuroscience?source=feed_text&epa=HASHTAG"><span class="_5afx"><span aria-label="hashtag" class="_58cl _5afz">#</span><span class="_58cm">neuroscience</span></span></a> <a class="_58cn" data-ft="{"type":104,"tn":"*N"}" href="https://www.facebook.com/hashtag/neurosurgery?source=feed_text&epa=HASHTAG"><span class="_5afx"><span aria-label="hashtag" class="_58cl _5afz">#</span><span class="_58cm">neurosurgery</span></span></a> <a class="_58cn" data-ft="{"type":104,"tn":"*N"}" href="https://www.facebook.com/hashtag/neurons?source=feed_text&epa=HASHTAG"><span class="_5afx"><span aria-label="hashtag" class="_58cl _5afz">#</span><span class="_58cm">neurons</span></span></a> <a class="_58cn" data-ft="{"type":104,"tn":"*N"}" href="https://www.facebook.com/hashtag/confreences?source=feed_text&epa=HASHTAG"><span class="_5afx"><span aria-label="hashtag" class="_58cl _5afz">#</span><span class="_58cm">confreences</span></span></a> <a class="_58cn" data-ft="{"type":104,"tn":"*N"}" href="https://www.facebook.com/hashtag/rome?source=feed_text&epa=HASHTAG"><span class="_5afx"><span aria-label="hashtag" class="_58cl _5afz">#</span><span class="_58cm">rome</span></span></a> <a class="_58cn" data-ft="{"type":104,"tn":"*N"}" href="https://www.facebook.com/hashtag/italy?source=feed_text&epa=HASHTAG"><span class="_5afx"><span aria-label="hashtag" class="_58cl _5afz">#</span><span class="_58cm">Italy</span></span></a> <a class="_58cn" data-ft="{"type":104,"tn":"*N"}" href="https://www.facebook.com/hashtag/june?source=feed_text&epa=HASHTAG"><span class="_5afx"><span aria-label="hashtag" class="_58cl _5afz">#</span><span class="_58cm">june</span></span></a><br />
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Anonymoushttp://www.blogger.com/profile/08717434777680943377noreply@blogger.com0tag:blogger.com,1999:blog-74280172020055059.post-33836664578776535962019-02-27T00:43:00.001-08:002019-02-27T00:43:20.979-08:00<div dir="ltr" style="text-align: left;" trbidi="on">
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<b><span style="color: purple;">NEUROLOGY 2019!!</span></b> We are glad to invite all academic medical professionals all over the world to the international conference. Don't miss the opportunity, Book your slots soon.<br />
#speaker slots available #Neurology #Neurologist #Neuroimmunology #Neurosurgery #Conference #Speaker #Rome #Italy #student<br />
Register soon to avail early bird offer.<br />
Have a look at <span style="color: blue;"><b>https://neurology.cmesociety.com/</b></span></div>
Anonymoushttp://www.blogger.com/profile/08717434777680943377noreply@blogger.com0tag:blogger.com,1999:blog-74280172020055059.post-42743207320952406832018-10-09T05:32:00.002-07:002018-10-09T05:32:32.084-07:00<div dir="ltr" style="text-align: left;" trbidi="on">
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About Conference : </h3>
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Pulsus Conferences takes its privilege to invite all the participants to the “<a href="https://neurology.cmesociety.com/call-for-abstracts" style="background-color: transparent; box-sizing: border-box; color: #3fa5ac; text-decoration-line: none;">4<span style="box-sizing: border-box; font-size: 10.5px; line-height: 0; position: relative; top: -0.5em; vertical-align: baseline;">th</span> International Conference on Neurology and Healthcare</a>” scheduled during <span style="box-sizing: border-box; font-weight: 700;">April 17-18, 2019 in Amsterdam</span>, <span style="box-sizing: border-box; font-weight: 700;">Netherlands</span> which will ensure the gathering of many healthcare professionals such as neuro specialists, neuro surgeons, neurologists and pioneers from the field of neuro robotics.</div>
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<a href="http://neurology.cmesociety.com/call-for-abstracts" style="background-color: transparent; box-sizing: border-box; color: #3fa5ac; text-decoration-line: none;">Neurology 2019</a> serves as an emerging platform to discuss about the recent advancements in neurology and healthcare which includes neuro robotics , deep brain simulation , neuro surgery , precision medicine for neural disorders and more…..</div>
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Neurology 2019 will be a grand event which is focused on the theme “<a href="http://neurology.cmesociety.com/call-for-abstracts" style="background-color: transparent; box-sizing: border-box; color: #3fa5ac; text-decoration-line: none;">Panoramic view of Neurology and Healthcare</a>” and ensures better advancements in healthcare for the future.</div>
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Pulsus Group is an internationally renowned peer-review publisher in scientific, technical, and medical journals established in the year 1984 with offices in Ontario , Canada and Hyderabad, India has acquired Andrew John Publishing and <a href="https://www.pulsusconference.com/neuroscience-meetings-workshops" style="background-color: transparent; box-sizing: border-box; color: #3fa5ac; text-decoration-line: none;">openaccessjournals.com</a> to expand its Open Access Publishing through its 50+ journals in association with 20+ International medical and scientific societies.</div>
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At pulsus group, It is our ideology to bring maximum exposure to our attendees, so we make sure that the event is a blend which covers professionals such as neurologists, neurosurgeons, neuro researchers, healthcare professionals from academia &industry making the<a href="https://neurology.cmesociety.com/call-for-abstracts" style="background-color: transparent; box-sizing: border-box; color: #3fa5ac; text-decoration-line: none;"> Neurology 2019 </a>a perfect platform.</div>
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<span style="box-sizing: border-box; font-weight: 700;">Why to Attend??</span></div>
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<a href="http://neurology.cmesociety.com/call-for-abstracts" style="background-color: transparent; box-sizing: border-box; color: #3fa5ac; text-decoration-line: none;">Neurology 2019</a> will enlighten the public with the importance of neurocare its advanced mode of treatments as well as the aspects of neuroscience. The conference also serves with trending works in the field of neurology and the recent research works by pioneer scholars. Neurology 2019 provides you a great platform to interact with renowned speakers, neurologists and neuro surgeons. <a href="https://neurology.cmesociety.com/call-for-abstracts/recent-advancements-in-neurology" style="background-color: transparent; box-sizing: border-box; color: #3fa5ac; text-decoration-line: none;">Recent advancements in neurolog</a>y, <a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-robotics" style="background-color: transparent; box-sizing: border-box; color: #3fa5ac; text-decoration-line: none;">neuro robotics</a> , <a href="https://neurology.cmesociety.com/call-for-abstracts/neurosurgery" style="background-color: transparent; box-sizing: border-box; color: #3fa5ac; text-decoration-line: none;">neuro surger</a>y, <a href="https://neurology.cmesociety.com/call-for-abstracts/recent-advancements-in-neurology" style="background-color: transparent; box-sizing: border-box; color: #3fa5ac; text-decoration-line: none;">precision medicines</a> are the trademark of this conference.</div>
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Neurology 2019 will be a stepping stone to the future healthcare with its eminent speakers and organizing committee members.</div>
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<span style="box-sizing: border-box; font-weight: 700;">Who should attend??</span></div>
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<li align="justify" style="box-sizing: border-box; margin-left: 21pt;">Neurologists, Neurosurgeons, Neuro physiologists, Pharmacists, Neurology Organizations & societies Pharmaceutical companies,Neuro and CNS drug Industries, Neuroscience associations & foundations, Neuro patients, Medical Students,Medical professors ,Bio medical-engineers, Research Scholars, Academic Scientists</li>
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pulsus conferenceshttp://www.blogger.com/profile/10796891539023352265noreply@blogger.com39tag:blogger.com,1999:blog-74280172020055059.post-31944213561069848432018-08-27T02:49:00.000-07:002018-08-27T02:49:28.199-07:00Neurology 2018 | Free Pass for 5 registrations | 50% discounts on each registration | Valids till September 5th | neurology@neuroconferences.net<div dir="ltr" style="text-align: left;" trbidi="on">
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Anonymoushttp://www.blogger.com/profile/08717434777680943377noreply@blogger.com20tag:blogger.com,1999:blog-74280172020055059.post-78250759494231717112018-08-26T22:51:00.001-07:002018-08-26T22:51:20.799-07:00#Avail 50% discounts on group registrations #Neurology2018 #Berlin #September17 Offer ends in September 3rd #Pulsusconferences Contact: neurology@neuroconferences.net #Meet your peer renowned speakers <div dir="ltr" style="text-align: left;" trbidi="on">
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Anonymoushttp://www.blogger.com/profile/08717434777680943377noreply@blogger.com0tag:blogger.com,1999:blog-74280172020055059.post-62652636946211706952018-07-19T02:53:00.001-07:002018-07-19T02:53:28.217-07:00PET Scan In Neurology <div dir="ltr" style="text-align: left;" trbidi="on">
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<b><span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;"><a href="https://neurology.cmesociety.com/call-for-abstracts/neurological-examination-imaging-radiology" target="_blank">Positron Emission Tomography (PET) Scan<o:p></o:p></a></span></b></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;">Positron emission tomography (PET) scans provide two- and <a href="https://neurology.cmesociety.com/call-for-abstracts/neurological-examination-imaging-radiology" target="_blank">three-dimensional pictures</a> of brain activity by measuring radioactive isotopes that are injected into the bloodstream. <a href="https://neurology.cmesociety.com/call-for-abstracts/neurological-examination-imaging-radiology" target="_blank">PET</a> scans of the brain are used to detect or highlight tumors and diseased tissue, measure cellular and/or tissue metabolism, show blood flow, evaluate patients who have seizure disorders that do not respond to medical therapy and patients with certain memory disorders, and determine <a href="https://neurology.cmesociety.com/" target="_blank">brain</a> changes following injury or drug abuse, among other uses. <o:p></o:p></span></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;">PET may be ordered as a follow-up to a <a href="https://neurology.cmesociety.com/call-for-abstracts/neurological-examination-imaging-radiology" target="_blank">CT or MRI </a>scan to give the physician a greater understanding of specific areas of the brain that may be involved with certain problems. Scans are conducted in a hospital or at a testing facility, on an outpatient basis. A low-level radioactive isotope, which binds to chemicals that flow to the brain, is injected into the bloodstream and can be traced as the brain performs different functions. <o:p></o:p></span></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;">The patient lies still while overhead sensors detect gamma rays in the body’s tissues. A computer processes the <a href="https://neurology.cmesociety.com/" target="_blank">information </a>and displays it on a video monitor or on film. Using different compounds, more than one brain function can be traced simultaneously. <o:p></o:p></span></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;">PET is painless and relatively risk-free. Length of test time depends on the part of the body to be scanned. PET <a href="https://neurology.cmesociety.com/call-for-abstracts/neurological-examination-imaging-radiology" target="_blank">scans</a> are performed by skilled technicians at highly sophisticated medical facilities.<o:p></o:p></span></div>
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<b><span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;"><a href="https://neurology.cmesociety.com/" target="_blank">Epilepsy</a><o:p></o:p></span></b></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;">The French investigators performed F-18 fluoro-L-dopa (FDOPA) <a href="https://neurology.cmesociety.com/call-for-abstracts/neurological-examination-imaging-radiology" target="_blank">positron emission tomography </a>(PET) in patients with temporal lobe epilepsy (TLE) and compared the findings to those with fluorodeoxyglucose (FDG) PET This study was motivated by a prior observation that F-18 FDOPA uptake in basal ganglia is decreased in patients with refractory TLE. A correlation was observed between the localization of seizure focus hypometabolism and decreased FDOPA uptake in both the basal ganglia and the substantia nigra, suggesting that there is a dopamine involvement in TLE. In another study the impact of TLE duration on brain FDG PET pattern was investigated. A negative correlation was demonstrated between epilepsy duration and ipsilateral glucose metabolism and a positive correlation with the contralateral glucose metabolism. This observation suggested that duration of TLE correlates with asymmetric glucose metabolism in the temporal lobes possibly reflecting the compensatory increased metabolism in the more normal temporal lobe over time. <o:p></o:p></span></div>
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<b><span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;"><a href="https://neurology.cmesociety.com/" target="_blank">Dementia</a><o:p></o:p></span></b></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;">The Brazilian researchers compared the FDG PET brain glucose metabolism with Tc-99m ethylcysteinate dimer (ECD) single-photon emission computed tomography (SPECT) brain regional cortical blood flow in patients with Alzheimer dementia. This study showed that similar functional cerebral regions are involved on PET and SPECT in Alzheimer's disease, although PET seemed to be more powerful in depicting the extent and severity of the <a href="https://neurology.cmesociety.com/call-for-abstracts/neurological-examination-imaging-radiology" target="_blank">functional impairments. </a><o:p></o:p></span></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;">The impact of FDG PET on the diagnosis and clinical management of patients with dementia was reported by the investigators from the Kettering Medical Center in Kettering, Ohio. FDG PET scans were performed on 96 patients with suspected dementia or mild cognitive impairment. Referring physicians were also surveyed to report on whether and how results of the PET scan influenced patient management. The survey response rate was 76%. The survey indicated that PET changed the initial diagnosis to Alzheimer dementia in 26% and disease management in 27% of patients leading to initiation of anticholinergic drug therapy. <o:p></o:p></span></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;">There has also been a growing interest in imaging beta-amyloid deposits directly with PET in Alzheimer dementia. An Australian study evaluated the relationship between amyloid burden as assessed by Pittsburgh Compound-B (PIB) PET and cognitive decline in predominantly normal elderly population (age 73 ± 6 years). These investigators observed that subjects with declining cognition were more likely to show cortical PIB retention than in stable subjects, suggesting that amyloid deposition is not a part of normal aging and likely represents preclinical Alzheimer's disease (described as those up to 30% of otherwise normal persons who are over 75 years but show amyloid deposition at autopsy). The researchers from the University of Pennsylvania compared the amyloid imaging agents [F-18]3'-F-PIB and [C-11]PIB in patients with Alzheimer's disease and in healthy subjects. The F-18-labeled compound showed uptake and retention characteristics similar to those of C-11-labeled compound in the more important cortical brain regions with SUV in the range of 3.1 to 4.5. Another similar study corroborated this finding and concluded that the F-18-labeled PET ligand might permit wide application of the compound due to longer half life and more ease of distribution in comparison to the C-11-labeled compound. <o:p></o:p></span></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;">The potential benefit of contrast-enhanced PET-CT was compared to non-enhanced PET-CT for differentiation of brain tumor recurrence from radiation necrosis. In this study, 29% of recurrent tumors were missed on non-enhanced PET-CT and were identified correctly on the enhanced scan. Additionally contrast enhancement revealed enhancing lesions in the other areas of brain away from the immediate region of interest. However, the clinical significance of these findings was unclear. The authors concluded that contrast-enhanced PET-CT is more suited in this clinical setting than the more common current procedure of using non-enhance scans. <o:p></o:p></span></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;">The Belgian researchers evaluated the diagnostic utility of PET with F-18 fluorotyrosine (FTYR), as a marker of amino acid transport, for detection of skull base meningioma. All tumours showed high FTYR uptake with an average tumor to cortex ratio of 2.53 ± .35. The metabolic abnormality on PET extended beyond the magnetic resonance imaging (MRI) abnormality in 38% and was smaller in 8% of cases. The authors concluded that FTYR PET was useful for the detection of residual meningiomas of the skull base with almost in half of the cases the tumor extent as depicted on PET differing from that on MRI, clinical significance of which is currently undetermined. <o:p></o:p></span></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;">Non-FDG-based PET was highlighted in several presentations. The UCLA group evaluated PET with F-18 fluorothymidine (FLT), as a marker of cell proliferation, in a group of patients with brain tumor who were treated with anti-angiogenic agents such as bevacizumab.<sup><a href="https://www.blogger.com/null">]</a></sup> A 25% reduction in tumor FLT uptake was considered as metabolic response which was then compared to MRI and survival data. A multivariate analysis showed that FLT response was the most powerful predictor of survival with a lack of reduction of FLT uptake at 6 weeks after treatment initiation increasing the hazard ratio of death by 5-fold. In another corollary study with FLT, the same group of investigators employed a 3-comparment, 2-tissue kinetic model with metabolite and partial volume corrections to estimate the rate constants during treatment in patients with high grade brain tumors. Changes in the influx rate K and the SUV were linked to treatment response which in turn was correlated to patient outcome. <o:p></o:p></span></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;">The Japanese investigators compared C-11 acetate, C-11 methionine (MET), and FDG PET in 16 patients with primary and recurrent brain gliomas (5 low grade, 11 high grade). The sensitivities for low-grade and high-grade gliomas were, respectively, 60% and 100% for MET, 40% and 91% for acetate, and 0% and 40% for FDG. The mean SUV for low grade and high grade tumors were, respectively, 1.4 ± 0.4 and 3.1 ± 1.6 for acetate and 4.2 ± 0.2 and 8.3 ± 3.9 for FDG. There was no significant difference in the MET uptake between the low-grade and high-grade tumors. The authors concluded that although MET might not be able to differentiate the histologic grades, it is more sensitive than both FDG and acetate for tumor detection. Therefore this study suggested that multi-tracer PET may be helpful for a more comprehensive evaluation of patients with brain glioma, although the very low rate of FDG localization in the high-grade tumors in this study is atypical. <o:p></o:p></span></div>
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Anonymoushttp://www.blogger.com/profile/08717434777680943377noreply@blogger.com0tag:blogger.com,1999:blog-74280172020055059.post-13099840549150199802018-07-18T01:19:00.000-07:002018-07-18T01:19:19.707-07:00Behavioural Techniques | Memory Reconsolidation <div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;"><span style="color: #20124d;"><a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-ophthalmology" target="_blank">Visual perceptual skills </a>are updated by the process similar to <a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-psychiatry" target="_blank">memory reconsolidation</a>.<o:p></o:p></span></span></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;"><span style="color: #20124d;">New<a href="https://neurology.cmesociety.com/call-for-abstracts/recent-advancements-in-neurology" target="_blank"> research</a> concludes that humans’ ability to identify and categorize what they see is kept up-to-date by reactivating lessons learned and allowing them to become stable over time.<o:p></o:p></span></span></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;"><span style="color: #20124d;">A new <a href="https://neurology.cmesociety.com/" target="_blank">study </a>shows that updating visual perceptual skills — which humans rely on to recognize what they see, including potential threats, and ignore unimportant background — is an active process with many similarities to the way they stabilize memories.<o:p></o:p></span></span></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;"><span style="color: #20124d;">Published in <a href="https://neurology.cmesociety.com/call-for-abstracts/neurological-aspects-in-health-care" target="_blank">Nature Human Behavior</a>, the study led by Brown University researchers tested whether memory reconsolidation, observed in animals, occurs in humans and whether it impacts skill learning. <o:p></o:p></span></span></div>
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<span style="color: #20124d;"><span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;">In animals, when a new memory is formed, that memory is fragile until time passes and the <a href="https://neurology.cmesociety.com/" target="_blank">memory</a> is consolidated. When memories are recalled or reactivated, they become temporarily unstable and vulnerable to change until they become stable again, shortly </span>afterward<span style="font-family: "Times New Roman", serif; font-size: 14pt;">.</span></span></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;"><span style="color: #20124d;">Using <a href="https://neurology.cmesociety.com/call-for-abstracts/neurological-aspects-in-health-care" target="_blank">behavioral </a>techniques and new <a href="https://neurology.cmesociety.com/call-for-abstracts/neurological-examination-imaging-radiology" target="_blank">brain imaging tools</a>, the study provides evidence that memory reconsolidation takes place in humans and that it underlies an important skill — visual perceptual learning.<o:p></o:p></span></span></div>
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<i><span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;"><span style="color: #20124d;">“This may explain why practice makes your skill and memory better, if you consider practice as a series of reactivations, increasing the level of plasticity again and again.”<o:p></o:p></span></span></i></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;"><span style="color: #20124d;">“We performed this study because it is controversial whether reactivation makes already consolidated memory fragile again and whether this occurs in humans,” said Yuka Sasaki, a professor of cognitive, linguistic and psychological science at Brown. “If such reactivation and reconsolidation are true functions of the brain, they should also occur in human vision.”<o:p></o:p></span></span></div>
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<span style="color: #20124d;"><span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;">Sasaki and her colleagues, including Takeo Watanabe, a professor of cognitive and linguistic science at Brown, trained study participants to recognize a blurred-stripe image, called a Gabor stimulus, as distinct from random dots. The next day, subjects were briefly tested to recall the skill they learned. They were then trained to find a new Gabor stimulus whose position was the same as the original one but whose orientation was different,</span><span style="font-family: "Times New Roman", serif; font-size: 14pt;">immediately afterwards or 3.5 hours later. On the third day, subjects were asked to practice finding the original Gabor stimulus.</span></span></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;"><span style="color: #20124d;">They found that the subjects who learned the altered Gabor stimulus immediately after looking at the original Gabor stimulus had significant trouble finding the original blurred stripe, suggesting that the reactivated memory was vulnerable to interference from new learning.<o:p></o:p></span></span></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;"><span style="color: #20124d;">But the subjects who had an interval of 3.5 hours between practicing the original test and the altered Gabor stimuli performed much better. This suggests that the subjects who had more time for their memories to reconsolidate were better able to cement their visual perceptual learning.<o:p></o:p></span></span></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;"><span style="color: #20124d;">These results reveal two important findings, the researchers said: Visual perceptual learning can undergo reconsolidation. And the reconsolidation window closes sometime before 3.5 hours after the initial recall. The results also suggest that consolidation and reconsolidation have similar influences on behavior.<o:p></o:p></span></span></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;"><span style="color: #20124d;">Sasaki and her colleagues also wanted to discover whether reconsolidation is underpinned by the same changes in brain activity. They used magnetic resonance spectroscopy (MRS) to measure concentrations in the excitatory neurotransmitter glutamate and in the inhibitory neurotransmitter GABA during consolidation and reconsolidation.<o:p></o:p></span></span></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;"><span style="color: #20124d;">A different group of participants again practiced the visual perception task or a control task that would not result in new learning. The next day, MRS was used to measure the visual area’s excitatory/inhibitory ratio both before and after the recall test as well as 3.5 hours afterwards.<o:p></o:p></span></span></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;"><span style="color: #20124d;">Immediately after memory reactivation, when the memory was unstable and changeable, there was a significant increase in the excitatory/inhibitory ratio (a decrease of inhibition compared to excitation). Importantly, once the reconsolidation window had closed and the memory was re-stabilized, the amount of excitation/inhibition returned to baseline levels. This suggests that the changeability of the old memory was driven by a decrease in inhibition, similar to the excitation/inhibition ratio for consolidation.<o:p></o:p></span></span></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;"><span style="color: #20124d;">The researchers also investigated whether the consolidation and reconsolidation of learned skills takes place according to similar timelines. They trained participants in a visual perception learning task and re-tested their memory either 3.5 hours after learning (consolidation group) or 3.5 hours after a recall test the next day (reconsolidation group). They found that both groups showed similar accuracy in the task 3.5 hours following learning or reactivation. This led them to conclude that both consolidation and reconsolidation occur over a similar amount of time.<o:p></o:p></span></span></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;"><span style="color: #20124d;">“This may explain why practice makes your skill and memory better, if you consider practice as a series of reactivations, increasing the level of plasticity again and again,” Sasaki said.<o:p></o:p></span></span></div>
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<span style="font-family: "Times New Roman",serif; font-size: 14.0pt; line-height: 107%;"><span style="color: #20124d;">By showing that <a href="https://neurology.cmesociety.com/" target="_blank">visual brain area</a>s are highly excitable following memory reactivation, Sasaki and her colleagues shed light on how new information is incorporated into the memory. And by providing evidence of the role of memory destabilization and reconsolidation in visual perceptual learning, the researchers offer insights into how the brain learns and refines new skills, keeping humans able to adapt in a changing world.<o:p></o:p></span></span></div>
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Anonymoushttp://www.blogger.com/profile/08717434777680943377noreply@blogger.com0tag:blogger.com,1999:blog-74280172020055059.post-41863985142918101802018-07-17T01:06:00.000-07:002018-07-17T01:06:59.311-07:00Levels of Dopamine | Parkinsons Disease | Towards A Better Tomorrow | Neurology 2018 <div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">Levels of Dopamine | Parkinsons Disease | Towards A Better Tomorrow | Neurology 2018 </span></h4>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">Arvid Carlsson, the Swedish <a href="https://neurology.cmesociety.com/organizing-committee" target="_blank">neuroscientist</a> and Nobel laureate, died on June 29, 2018 at the age of 95. He had devoted his life to understanding how the brain works and was awarded the Nobel for his research into<a href="https://neurology.cmesociety.com/abstract-submission" target="_blank"> dopamine</a> – an important chemical found in the brain.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">So what is dopamine, and why did finding out about it merit the Nobel Prize?<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;"><a href="https://neurology.cmesociety.com/call-for-abstracts" target="_blank">Dopamine</a> is a simple chemical, made in the body from an amino acid called tyrosine. Despite its simplicity, it plays an important role as a <a href="https://neurology.cmesociety.com/call-for-abstracts/neurosurgery" target="_blank">neurotransmitter</a> – chemicals that brain cells use to<a href="https://neurology.cmesociety.com/call-for-abstracts/neurological-aspects-in-health-care" target="_blank"> communicate</a> with one another.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;"><a href="https://neurology.cmesociety.com/" target="_blank">Dopamine: Methods and Protocols</a></span></h3>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">What Carlsson did was to reveal exactly how significant dopamine is to the function of the brain. Before his research, most people thought that dopamine was just a precursor of a <a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-psychology" target="_blank">brain hormone</a> called noradrenaline. By decreasing dopamine levels in the brains of rabbits in his lab in Gothenburg, Carlsson was able to show that if you don’t have the right level of dopamine in your brain, the circuits that determine how the brain controls movement don’t work properly.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">Although Carlsson was investigating basic <a href="https://neurology.cmesociety.com/" target="_blank">neuroscience</a>, it wasn’t long before scientists and doctors realised that there were similarities between the problems with movement that Carlsson had observed in rabbits and the symptoms of Parkinson’s disease.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;"><a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-psychiatry" target="_blank">Parkinson’s disease</a> is a <a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-psychiatry" target="_blank">neurodegenerative disorder,</a> a type of disease where increasing numbers of brain cells die over time, causing patients to develop problems with their movement, including uncontrollable shaking, slowed movement and sudden freezing.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">Following on from Carlsson’s research, doctors soon realised that if they examined the brains of people with Parkinson’s there was much less dopamine than you would find in a healthy brain. This is because the cells that make and use dopamine in the brain, dopaminergic neurons, are the cells that die in Parkinson’s disease.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">This led researchers to propose a simple solution. If the symptoms of Parkinson’s are caused by too little dopamine, why not boost these levels, with a dopamine pill or injection, to help the brain work again?<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;"><a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-psychiatry" target="_blank">Awakenings</a></span></h4>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">Unfortunately, this approach didn’t work, as dopamine isn’t able to cross from the bloodstream into the brain. But providing people with Parkinson’s a precursor to dopamine, a chemical called levodopa that can get into the brain and is converted into dopamine, did work and provided relief from many of the symptoms of Parkinson’s. This was immortalised in the book Awakenings, written by neurologist Oliver Sacks and later made into a film starring Robin Williams and Robert De Niro.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">In Awakenings, patients with post-encephalitic <a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-psychiatry" target="_blank">Parkinsonism </a>(a viral disease similar to Parkinson’s disease) who were treated with levodopa, had almost miraculous improvements in their symptoms.<o:p></o:p></span></div>
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</v:shape><![endif]--><!--[if !vml]--><img alt="The Conversation" height="1" src="file:///C:/Users/NEUROL~1/AppData/Local/Temp/msohtmlclip1/01/clip_image001.gif" v:shapes="Picture_x0020_3" width="1" /><!--[endif]--></span><span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">Unfortunately, levodopa, and other drugs that target dopamine levels in the brain, only treat the symptoms of Parkinson’s, they don’t slow down the loss of brain cells that underlie the disease. Despite this, and some serious side effects, they remain the frontline drug in our fight against the disease. But we wouldn’t have these frontline drugs if it wasn’t for the important work that Carlsson conducted in the 1950s, and for which he shared the Nobel Prize for Physiology or Medicine in 2000.<o:p></o:p></span></div>
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Anonymoushttp://www.blogger.com/profile/08717434777680943377noreply@blogger.com2tag:blogger.com,1999:blog-74280172020055059.post-29926376476462381432018-07-16T01:06:00.000-07:002018-07-16T01:06:52.830-07:00High Blood Pressure | Neuro-Cognition | Communication | Neurons | Neurology2018 <div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="font-family: "times new roman" , serif; font-size: 16.0pt; line-height: 107%;"><a href="https://neurology.cmesociety.com/" target="_blank">Scientists explore how high blood pressure hurts cognition</a><o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">Researchers report impairments in the <a href="https://neurology.cmesociety.com/" target="_blank">neuroprotective</a> communication between <a href="https://neurology.cmesociety.com/abstract-submission" target="_blank">neural blood vessels</a>, astrocytes and <a href="https://neurology.cmesociety.com/call-for-abstracts" target="_blank">neurons</a> may be an early factor in how high blood pressure may impair cognitive function.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">The squeeze high <a href="https://neurology.cmesociety.com/poster-presentation" target="_blank">blood pressure </a>puts on fragile blood vessels in the brain appears to disrupt a normal, protective process that balances the blood flowing to our brains with the activity of our resting neurons.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">In the face of hypertension, as blood flow decreases, neuron-nurturing brain cells called astrocytes may instead tell neurons to increase their activity<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">These impairments in the <a href="https://neurology.cmesociety.com/call-for-abstracts/neurology" target="_blank">neuroprotective communication </a>between brain blood vessels, astrocytes and neurons may be an early factor in how hypertension impairs cognitive function.<o:p></o:p></span></div>
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<i><span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">Neurons don’t have energy reserves, so their activity is dependent on continuous blood flow.<o:p></o:p></span></i></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">Untreated hypertension can lead to <a href="https://neurology.cmesociety.com/call-for-abstracts/neuromedicine" target="_blank">cognitive impairment</a> but exactly how it happens, we don’t really know. We need to understand the window of change or shift in function in all these different cells. What exactly is happening, in what order and how fast?<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">By the time patients are symptomatic, a lot of the physiology of the vasculature has deteriorated so the question is: How can we diagnose impairments in vascular function way before that, years before cognitive impairments are established and become symptomatic.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">Regulation of blood flow, both up and down, is a normal, relentless function in our bodies. Certainly, that is true in the closed confines of the skull where there is literally little wiggle room, plus the brain just doesn’t like extreme ups or downs. In fact, fine adjustments are even made each time we stand up or sit. Your brain autoregulates to maintain flow relatively constantly,which is a good thing.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">Huge increases in flow, for example, can result in dangerous swelling, particularly if blood pressure also happens to go up. Conversely, lower pressure and less blood flow mean less energy for neurons, which pretty much operate with an empty cupboard that requires the continuous flow of blood and the oxygen and nutrients it contains to function.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">Neurons don’t have energy reserves so their activity is dependent on continuous blood flow. That’s why brain cells can die so quickly in the aftermath of a stroke or head trauma and why they probably don’t function well with chronic hypertension. A lot of these things get activated as a protective mechanism, but chronically they can shift into being more deleterious.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">High blood pressure makes the thin-walled parenchymal arterioles that carry the blood neurons need constrict, so they carry less blood. Astrocytes, whose finger-like appendages cover most of the surface of these blood vessels, sense the increased pressure.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">They had shown that the increased arteriole constriction they sense appears to trigger an increase in calcium inside the astrocytes, an indicator that their activity level has gone up. The increased calcium can lead to many things but in this case, researchers think the calcium overload turns normally protective astrocytes bad. They appear to both increase constriction – apparently by tightening their grip on the blood vessels – and promote inflammation.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">It can shift who these astrocytes become, One of the many things they are further exploring is what happens, in turn, to the neurons.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">They have evidence that one message neurons are not getting from these altered astrocytes is to reduce their resting activity even though less sustenance is available, creating an unhealthy balance for the brain.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">A lot of these things get activated as a protective mechanism, but chronically they can shift into being more deleterious.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">Over time, high blood pressure also results in a remodelling and stiffening of previously agile blood vessel walls so there is even less blood flowing. The unhealthy remodelling further alters the protective conversations the vessels, astrocytes and neurons should be having.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">Eventually, communication appears to get reset so that resting blood flow and resting neuronal activity that enable basics like breathing are out of balance. There is a rightward shift,<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">This imbalance may also eventually decrease the normal ability to increase blood flow and neuronal activity when it’s time to solve a math problem or to have that significant conversation with a friend.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">To better understand what goes bad, they are looking again at how a healthy balance happens and what hypertension does to it.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">They are looking at what happens to calcium levels inside astrocytes in response to higher and lower pressures in the parenchymal arterioles in the brains of both normal mice and those that already have impaired blood flow. They also want to know what precisely mediates any change.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">They are looking, both in brain slices and lab animals, at how pressure and flow changes in the fragile arterioles impact the resting activity of neurons in both the presence and absence of cardiovascular disease.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">They want to know if at least one way a healthy balance occurs is by astrocytes recruiting GABAergic <a href="https://neurology.cmesociety.com/abstract-submission" target="_blank">interneurons</a>, which are known to play a role in inhibiting neuronal activity. They also are looking at which specific interneuron subtype drives neuronal response in the face of cardiovascular disease, suspecting it instead drives neuronal activity upward.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">High blood pressure is a well-established risk factor for stroke and for cognitive function, in fact, a recent study published in <i>Frontiers in Aging <a href="https://neurology.cmesociety.com/call-for-abstracts/neuromedicine" target="_blank">Neuroscience</a></i><a href="https://neurology.cmesociety.com/call-for-abstracts/neuromedicine" target="_blank">indicates </a>that hypertension accelerates <a href="https://neurology.cmesociety.com/call-for-abstracts/neuromedicine" target="_blank">Alzheimer’s</a> development and that midlife control of high pressures may delay onset.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">Rest is relative for neurons, which always are working at some level to maintain our basic functions. In fact, the majority of the brain’s energy goes to maintain resting activity that enables basics like breathing.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">Functionally evoked changes in blood flow – like when you are actively thinking or doing – temporarily override cerebral autoregulation that in a healthy state balances basal blood flow and resting neuronal activity.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">Source: AU<o:p></o:p></span></div>
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Anonymoushttp://www.blogger.com/profile/08717434777680943377noreply@blogger.com0tag:blogger.com,1999:blog-74280172020055059.post-31860158364076436032018-07-12T02:32:00.000-07:002018-07-12T02:32:51.151-07:00Recent Advancements | Research | Quantum Dots | Parkinson's & Alzheimer's | Neurology 2018 <div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="color: #073763;"><a href="https://neurology.cmesociety.com/call-for-abstracts/recent-advancements-in-neurology" target="_blank">Quantum Dots</a> | Reduced Symptoms | <a href="https://neurology.cmesociety.com/" target="_blank">Parkinsons Disease & Alzheimer's</a> | <a href="https://neurology.cmesociety.com/call-for-abstracts/recent-advancements-in-neurology" target="_blank">Research Areas </a></span></div>
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<span style="color: #073763;">Tiny particles called quantum dots reduce symptoms in mice primed to develop a type of <a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-psychiatry" target="_blank">Parkinson’s disease</a> and also block the formation of the toxic protein clumps in <a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-psychiatry" target="_blank">Alzheimer’s</a>. They could one day be a novel treatment for these brain disorders, although tests in people are some years away.<o:p></o:p></span></div>
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<span style="color: #073763;">Quantum dots are just a few nanometres in size – so small they become subject to some of the strange effects of quantum physics. They have useful electronic and <a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-intensive-care-unit" target="_blank">fluorescent properties </a>and are found in some <a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-intensive-care-unit" target="_blank">TV screens and LED lights.</a><o:p></o:p></span></div>
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<span style="color: #073763;">Unlike most medicines, their tiny size means they can pass from the bloodstream into the brain. Byung Hee Hong of Seoul National University in South Korea and his colleagues wondered if they would affect the molecules involved in Parkinson’s or other brain disorders.<o:p></o:p></span></div>
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<span style="color: #073763;">Parkinson’s disease involves gradually worsening tremors and <a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-robotics" target="_blank">movement problems</a>. It is thought to be caused by a protein called synuclein found in nerve cells folding into the wrong shape, which triggers a chain reaction of misfolding in nearby synuclein molecules. This leads to a build-up of long strands or “fibrils” of the protein, killing neurons.<o:p></o:p></span></div>
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<b><span style="color: #073763;"><a href="https://neurology.cmesociety.com/call-for-abstracts/recent-advancements-in-neurology" target="_blank">Quantum surprise</a><o:p></o:p></span></b></div>
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<span style="color: #073763;">Hong’s team found that in a dish, quantum dots made from graphene – a form of carbon – bind to synuclein, and not only stop it from clumping into fibres, but also cause existing fibres to break up into individual molecules. “We didn’t expect the quantum dots to induce disaggregation of fibrils,” says Hong.<o:p></o:p></span></div>
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<span style="color: #073763;">Next, the team injected quantum dots into mice dosed with fibrils, which normally trigger gradually worsening movement problems. Six months later, the mice showed improvement on two different physical tests.<o:p></o:p></span></div>
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<span style="color: #073763;">If the treatment affects people the same way, Hong says it is unclear how much benefit this would bring. “It’s hard to translate the results in mice to actual patients, whose systems are way more complicated. But we do believe quantum dots can make positive impacts to some extent.”<o:p></o:p></span></div>
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<span style="color: #073763;">Another team has found that quantum dots show promise for Alzheimer’s disease; in a similar fashion, they bind to a protein called amyloid, and reduce it from clumping together, a process thought to be involved in this dementia. However, tests in an animal version of Alzheimer’s haven’t yet been reported.<o:p></o:p></span></div>
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<span style="color: #073763;">“This might be a universal effect on any kind of fibrillation process related to disease,” says Hong. His team is investigating using quantum dots in Alzheimer’s and motor neuron disease – the condition that affected Stephen Hawking – which also involves protein clumping.<o:p></o:p></span></div>
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<span style="color: #073763;">Sebastien Paillusson of King’s College London, who was not involved in the work, says the findings in mice are promising, but should not raise anyone’s hopes until the approach has been tested in people. “Unfortunately in Parkinson’s, there have been a lot of compounds shown to work in mice but not in humans.”<o:p></o:p></span></div>
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<span style="color: #073763;">Paillusson added, though, that it was unusual for anything to reverse the fibre-forming process. “This is a very novel approach.”<o:p></o:p></span></div>
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<span style="color: #073763;">Hong says if safety tests in animals go well, they hope to start trials in people in about two years<o:p></o:p></span></div>
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Anonymoushttp://www.blogger.com/profile/08717434777680943377noreply@blogger.com2tag:blogger.com,1999:blog-74280172020055059.post-29724060240604539672018-07-11T02:44:00.002-07:002018-07-11T02:44:46.223-07:00Neurotransmitter | Noradrenaline | Sensory Perceptions | Brain | Neurology 2018 | Berlin <div dir="ltr" style="text-align: left;" trbidi="on">
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<a href="https://neurology.cmesociety.com/" target="_blank">Neurotransmitter </a>| Noradrenaline | <a href="https://neurology.cmesociety.com/abstract-submission" target="_blank">Sensory Perceptions</a> | Brain | <a href="https://neurology.cmesociety.com/" target="_blank">Neurology2018</a> | <a href="https://neurology.cmesociety.com/venue-hospitality" target="_blank">Berlin </a></h3>
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<i><br /></i><i>A new study reveals <a href="https://neurology.cmesociety.com/call-for-abstracts" target="_blank">noradrenaline</a> plays a vital role in early stages of perception. Researchers report later processing of visual information occurs in the cerebral cortex and is affected by noradrenaline to determine if an image will enter our stream of <a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-psychology" target="_blank">consciousness</a>.</i></h4>
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A new study published in <i>Current Biology</i> suggests that noradrenaline, a <a href="https://neurology.cmesociety.com/call-for-abstracts/neuromedicine" target="_blank">neurotransmitter</a> responsible for arousal in the brain, plays a vital role in our early sensory perceptions of the world.<o:p></o:p></div>
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Until now, medical science believed that noradrenaline is involved in alertness, stress, attention and decision making, says senior author Dr. Yuval Nir, of TAU’s Sackler Faculty of Medicine and Sagol School of <a href="https://neurology.cmesociety.com/" target="_blank">Neuroscience</a>. Our study shows that, in fact, noradrenaline plays a vital role in earlier stages of perception, determining our ability to perceive events around us.<o:p></o:p></div>
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The research was jointly led by Dr. Hagar Gelbard-Sagiv and Efrat Magidov of TAU’s Sackler Faculty of Medicine and Sagol School of <a href="https://neurology.cmesociety.com/" target="_blank">Neuroscience,</a><o:p></o:p></div>
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The scientists ran a series of experiments on 30 participants at the Sagol Brain Institute at Tel Aviv Medical Center. Subjects took part in three different sessions in which they received (1) drugs that lowered noradrenaline levels; (2) drugs that increased those levels; or (3) a placebo. After taking the medication, the participants were asked to perform visual tasks such as detecting and discriminating between low-contrast images, while the researchers measured their brain activity by EEG or fMRI. The researchers hoped to determine how various levels of noradrenaline affected visual perception and the way the brain responds to images.<o:p></o:p></div>
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We determined that noradrenaline affected the participants’ ability to detect low-contrast images. Even though the images were identical in each case, their visibility changed across sessions. We could predict whether the subjects could perceive those images by examining the levels of noradrenaline in their systems,”says Dr. Gelbard-Sagiv.<o:p></o:p></div>
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Our measurements of brain activity show that the first stages of visual processing are quite automatic, but late processing in the cerebral cortex is affected by noradrenaline and determines if an image will enter our stream of consciousness,” adds Magidov.<o:p></o:p></div>
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“Many people suffer from difficulties in initiating and maintaining sleep,” Dr. Nir concludes. “We hope to follow up on these results and test whether noradrenaline also determines if sensory stimuli such as sounds wake us up from sleep.<o:p></o:p></div>
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“We hope that in the future our findings will open new avenues for the development of better anesthetics and new tools for early detection of dangerous situations, such as lapses while driving or flying.”<o:p></o:p></div>
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<i>Source: AFTAU.</i><o:p></o:p></div>
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Anonymoushttp://www.blogger.com/profile/08717434777680943377noreply@blogger.com0tag:blogger.com,1999:blog-74280172020055059.post-11402653874639869942018-07-10T01:05:00.000-07:002018-07-10T01:05:50.900-07:00Nomenclature | Genetic Movement Disorders | Neurology 2018 | Neurology Conference 2018 <div dir="ltr" style="text-align: left;" trbidi="on">
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<b>A new nomenclature for <a href="https://neurology.cmesociety.com/call-for-abstracts/rehabilitation-process-in-neuromedicine" target="_blank">genetic movement disorders.</a><o:p></o:p></b></div>
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A Task Force was created by the International <a href="https://neurology.cmesociety.com/" target="_blank">Parkinson</a> and <a href="https://neurology.cmesociety.com/" target="_blank">Movement Disorders</a> Society with the aim of analysing apparent problems and providing solutions regarding the current nomenclature of genetic movement disorders. <o:p></o:p></div>
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Their <a href="https://neurology.cmesociety.com/help-desk" target="_blank">suggestions</a> have been published,<o:p></o:p></div>
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<!--[if !supportLists]-->1.<span style="font-size: 7pt; font-stretch: normal; font-variant-east-asian: normal; font-variant-numeric: normal; line-height: normal;"> </span><!--[endif]-->Aim to tackle several drawbacks of the current locus assignment system, such as 1) the inability to distinguish <a href="https://neurology.cmesociety.com/call-for-abstracts" target="_blank">disease-causing</a> mutations from genetic risk factors, 2) inconsistent associations with phenotype, 3) failure to assign a locus symbol in some established movement disorders, 4) more than one symbol being assigned for the same disorder, 5) unconfirmed genotype-phenotype associations, 6) erroneous labels and 7) symbol designation in the absence of known locus or gene. <o:p></o:p></div>
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The proposed <a href="https://neurology.cmesociety.com/abstract-submission" target="_blank">nomenclature </a>suggests that a disorder should be listed only if the causative gene is already known (i.e. genetic testing is possible), and appropriate prefixes should be assigned according to the core phenotypic feature, followed by the causative gene (e.g. DYT-gene1, PARK-gene2, HSP-gene3). Thus, currently used locus numbers are eliminated from future medical terminology (e.g. DYT1, PARK6,…). Suggested designations derive from primary clinical phenomenology: genetically determined parkinsonism, dystonia, chorea, paroxysmal movement disorders, dominant cerebellar ataxia, and spastic paraplegia. <o:p></o:p></div>
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Two groups of genetically determined disorders are prefixed not according to phenotype but typical imaging instead: primary familial brain calcification (PFBC-gene1, PFBC-gene2,…) and neurodegeneration with brain iron accumulation (NBIA-gene1, NBIA-gene2,…). Rules have been defined for disorders featuring mixed core characteristics. Future work will focus on as yet not approached disorders such as myoclonus, as well as x-linked, recessive, and congenital ataxias.<o:p></o:p></div>
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For more details :-<a href="https://neurology.cmesociety.com/">https://neurology.cmesociety.com/</a></div>
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Anonymoushttp://www.blogger.com/profile/08717434777680943377noreply@blogger.com0tag:blogger.com,1999:blog-74280172020055059.post-87283173134962551352018-07-08T23:58:00.001-07:002018-07-08T23:58:24.172-07:00Obesity | Overweight | Condition After Brain Injury | Neurology 2018 <div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="font-family: "times new roman" , serif; font-size: 12pt; font-weight: normal; line-height: 107%;">The study included 7,287 adults with TBI who had undergone inpatient acute <a href="https://neurology.cmesociety.com/call-for-abstracts/rehabilitation-process-in-neuromedicine" target="_blank">rehabilitation</a>. Inpatient rehabilitation consists of intensive therapy, provided by a team of specialists, designed to improve physical and <a href="https://neurology.cmesociety.com/call-for-abstracts/rehabilitation-process-in-neuromedicine" target="_blank">mental functioning</a>. Care was provided by rehabilitation centers participating in the the Traumatic Brain Injury Model Systems (TBIMS) program, sponsored by the National Institute on Disability, Independent Living, and <a href="https://neurology.cmesociety.com/call-for-abstracts/rehabilitation-process-in-neuromedicine" target="_blank">Rehabilitation Research</a>.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 12pt; font-weight: normal; line-height: 107%;">About three-fourths of patients were men; the average age was 46 years. The relationship between body weight and functional and health outcomes was assessed from one to 25 years after TBI. At the most recent follow-up, 23 percent of TBI survivors were classified as obese, 36 percent as overweight, 39 percent as normal weight, and three percent as underweight.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 12pt; font-weight: normal; line-height: 107%;">Overweight and obesity were less likely for patients under age 30, as well as those aged 80 years or older. While the percentage of overweight patients was relatively stable, the obesity rate increased over time especially five years or longer after TBI.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 12pt; font-weight: normal; line-height: 107%;">Being overweight or obese was strongly associated with several chronic <a href="https://neurology.cmesociety.com/call-for-abstracts/neuromedicine" target="_blank">health conditions</a>, including high blood pressure, heart failure, and diabetes. Overweight/obese patients also rated themselves as having poorer general health. The frequency of seizures -- a common problem among TBI survivors was also related to differences in body weight and health status.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 12pt; font-weight: normal; line-height: 107%;">The overall rate of overweight/obesity in the TBI patients (59 percent) was lower than reported in the general US population (over 70 percent). This may be attributed to several reasons in need of further examination -- for example, a higher rate of health complications, rehospitalizations, medication side effects, or death among individuals who were already obese at the time of TBI and thus were excluded from the follow-up study.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 12pt; font-weight: normal; line-height: 107%;">Achieving and maintaining a healthy diet and engaging in regular physical activity following a TBI are critical goals for recovery, Dr. Dreer and coauthors write. During the early recovery period, patients may lose weight due to increased metabolic rate and other physical effects of TBI. In the later phases, weight gain may occur due to a wide range of factors including medical conditions, medications, cognitive or behavioural changes, physical limitations, and lack of transportation or other resources.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 12pt; font-weight: normal; line-height: 107%;">Based on the large-scale TBIMS database, the new study confirms that being overweight or obese is associated with significant health problems for survivors of moderate to severe TBI who require acute rehabilitation. The researchers note some important limitations of their study, including the lack of information on the timing of weight problems and associated health conditions.<o:p></o:p></span></div>
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<span style="font-family: "times new roman" , serif; font-size: 12.0pt; line-height: 107%;"><span style="font-weight: normal;">However, these findings do highlight the potential importance of surveillance, prevention, and management of weight and related health conditions during the years postinjury, Dr Dreer and colleagues conclude.</span></span><span style="font-family: "times new roman" , serif; font-size: 12pt;">Lifestyle and health behaviours related to weight gain will need to be a component of any proactive approach to managing TBI as a chronic health condition.</span></div>
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<span style="font-family: "times new roman" , serif; font-size: 12pt;">Submit your Abstract and join us:- </span><span style="text-align: left;"><span style="font-family: "times new roman" , serif;"><a href="https://neurology.cmesociety.com/abstract-submission">https://neurology.cmesociety.com/abstract-submission</a> </span></span></div>
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Anonymoushttp://www.blogger.com/profile/08717434777680943377noreply@blogger.com1tag:blogger.com,1999:blog-74280172020055059.post-64145466596638547692018-07-07T00:05:00.003-07:002018-07-07T02:15:02.683-07:00Influential Speakers | Talks | Neurology 2018 | Neurology Conference 2018 | Berlin | Germany<div dir="ltr" style="text-align: left;" trbidi="on">
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<a href="https://neurology.cmesociety.com/poster-presentation">Influential Speakers </a>| <a href="https://neurology.cmesociety.com/abstract-submission" target="_blank">Talks </a>| <a href="https://neurology.cmesociety.com/">Neurology 2018</a> | <a href="https://neurology.cmesociety.com/">Neurology Conference 2018</a> | <a href="https://neurology.cmesociety.com/venue-hospitality">Berlin</a> | <a href="https://neurology.cmesociety.com/venue-hospitality">Germany</a></h4>
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<span style="background-color: white; color: #404040; font-family: "roboto" , "arial" , sans-serif; font-size: 13px;"><i>4th International Conference on Neurology & Health Care</i></span></h2>
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<a class="ot-hashtag aaTEdf" href="https://plus.google.com/s/%23Theme/posts" rel="nofollow" style="background-color: white; color: #262626; cursor: pointer; font-family: Roboto, arial, sans-serif; font-size: 13px; font-weight: bold; text-decoration-line: none; transition: color 0.218s;">#Theme</a><span style="background-color: white; color: #404040; font-family: "roboto" , "arial" , sans-serif; font-size: 13px;">:<a href="https://neurology.cmesociety.com/" target="_blank"> Broader Outlook in the Field of Neurology and Health Care</a></span></h4>
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<span style="background-color: white; color: #404040; font-family: "roboto" , "arial" , sans-serif; font-size: 13px;">Date: </span><a class="ot-hashtag aaTEdf" href="https://plus.google.com/s/%23September/posts" rel="nofollow" style="background-color: white; color: #262626; cursor: pointer; font-family: Roboto, arial, sans-serif; font-size: 13px; font-weight: bold; text-decoration-line: none; transition: color 0.218s;">#September</a><span style="background-color: white; color: #404040; font-family: "roboto" , "arial" , sans-serif; font-size: 13px;"> 17-18, 2018 </span></h4>
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<span style="background-color: white; color: #404040; font-family: "roboto" , "arial" , sans-serif; font-size: 13px;">Conference Venue: </span><a class="ot-hashtag aaTEdf" href="https://plus.google.com/s/%23Berlin/posts" rel="nofollow" style="background-color: white; color: #262626; cursor: pointer; font-family: Roboto, arial, sans-serif; font-size: 13px; font-weight: bold; text-decoration-line: none; transition: color 0.218s;">#Berlin</a><span style="background-color: white; color: #404040; font-family: "roboto" , "arial" , sans-serif; font-size: 13px;">, Germany</span></h4>
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Anonymoushttp://www.blogger.com/profile/08717434777680943377noreply@blogger.com0tag:blogger.com,1999:blog-74280172020055059.post-52101954332806320672018-07-06T00:14:00.000-07:002018-07-06T00:14:09.084-07:00Depression | Brain Stimulation | ECT | Neurology2018| Neurology Conference 2018<div dir="ltr" style="text-align: left;" trbidi="on">
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<b><a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-psychology" target="_blank">Depression </a>| <a href="https://neurology.cmesociety.com/call-for-abstracts/neurosurgery" target="_blank">Brain Stimulation</a><i> |</i> ECT | <a href="https://neurology.cmesociety.com/" target="_blank">Neurology2018</a> | <a href="https://neurology.cmesociety.com/" target="_blank">Neurology Conference 2018</a></b></h3>
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Researchers report both those who received voluntary and involuntary <a href="https://neurology.cmesociety.com/call-for-abstracts/recent-advancements-in-neurology" target="_blank">electroconvulsive therapy </a>reported their symptoms were much improved following treatment.<o:p></o:p></div>
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The findings, which have just been published in the July issue of the journal <a href="https://neurology.cmesociety.com/call-for-abstracts/neurosurgery" target="_blank"><i>Brain Stimulation</i>,</a> are based on the largest study of its kind internationally and one of very few studies to report on people requiring involuntary treatment, who are rarely able to take part in clinical research. The results provide reassurance for people who have had involuntary ECT, their families and healthcare providers, according to Professor of Psychiatry Declan McLoughlin from Trinity’s Department of Psychiatry and Trinity Institute of <a href="http://neuroscience./">Neuroscience.</a><o:p></o:p></div>
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The study found that people who have involuntary ECT were more severely unwell before treatment than those having voluntary ECT and were more likely to have<a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-psychology" target="_blank"> psychotic</a> symptoms such as hallucinations and delusions, and have more physical deterioration as a result of severe self-neglect.</div>
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<a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-psychology" target="_blank">Depression</a> is one of the leading causes of disability worldwide. People who suffer from severe depression may lose the capacity to make decisions and require treatment under mental health law in order to recover. ECT is the most effective acute treatment for severe depression and is sometimes administered as an involuntary treatment. In Ireland, approximately fifty people require involuntary ECT each year.<o:p></o:p></div>
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The research team, led by Professor McLoughlin, studied the records of five years of involuntary ECT treatment at St Patrick’s Mental Health Services, Dublin, Ireland. The team reported on 48 involuntary ECT courses and compared these with 96 courses of voluntary ECT administered to people of the same age and sex at the same time.<o:p></o:p></div>
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The results shed light on a group about which little is known and provide a stronger evidence base for patients receiving involuntary ECT under the provisions of mental health legislation, according to Professor McLoughlin.<o:p></o:p></div>
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People who require involuntary ECT are among the most severely unwell in our mental health services. Yet, because they generally lack decision-making capacity and cannot take part in research, we do not know for sure if we can apply research advances to persons having involuntary ECT. Our knowledge of how best to use ECT to help someone recover from severe depression is based on research samples comprised entirely of people choosing to have voluntary ECT.<o:p></o:p></div>
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Our results are reassuring for people who have had involuntary ECT and their families. It’s also a relief to mental health professionals to know that the research results on which we base treatment decisions for voluntary treatment can now be used with greater confidence to also guide treatment for people having involuntary ECT.”<o:p></o:p></div>
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He cautioned, however, that “although ECT is a safe and highly effective evidence-based treatment, ongoing research is essential to understand who will benefit most from the treatment, and how to help people with depression stay well after recovery”.<o:p></o:p></div>
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Anonymoushttp://www.blogger.com/profile/08717434777680943377noreply@blogger.com0tag:blogger.com,1999:blog-74280172020055059.post-52753623917164125332018-07-04T23:32:00.003-07:002018-07-04T23:35:37.767-07:00Neurology Conference | Parkinson's disease | Intestine | Research Topics | Neurology 2018 | Call For Papers | <div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="color: #351c75;"><a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-psychiatry" target="_blank">Parkinson's disease </a>| Intestine | <a href="https://neurology.cmesociety.com/call-for-abstracts" target="_blank">Research Topics </a> | Neurology 2018 </span></h3>
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<span style="color: #351c75;">When we think of <a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-psychiatry" target="_blank">Parkinson's disease</a> we typically associate it with its motor complications (difficulty initiating movement, stiffness, tremor, instability in posture). These symptoms are caused by the death of <a href="https://neurology.cmesociety.com/call-for-abstracts/neuromedicine" target="_blank">dopamine-producing neurons</a>, located in a region of the brain called the substantia nigra. The gradual death of these neurons occurs over the course of several years. When patients have movement difficulties, it is estimated that more than 60% of their dopaminergic neurons have been irreversibly affected.<o:p></o:p></span></div>
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<span style="color: #351c75;">In the early stages of the disease, other types of complications have been observed, including constipation and gastrointestinal disorders. Constipation is one of the most common non-motor symptoms of the disease. It was documented for more than 200 years by James Parkinson in the first report of the disease. In 2010, researchers from the National Institute of <a href="https://neurology.cmesociety.com/" target="_blank">Neurology </a>and <a href="https://neurology.cmesociety.com/call-for-abstracts/neurosurgery" target="_blank">Neurosurgery </a>in Mexico City reported that 30% of Parkinson's patients studied suffer from gastrointestinal disorders.<o:p></o:p></span></div>
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<span style="color: #351c75;">In recent years, various investigations have linked Parkinson's Disease with an alleged origin in the intestine. This is due to the findings of a possible transmission of the intestine to the brain. Here I will present the main mechanisms that are proposed to explain this relationship between these parts of the body.<o:p></o:p></span></div>
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<span style="color: #351c75;">1. Transmission of the intestine to the brain<div class="separator" style="clear: both; text-align: center;">
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<span style="color: #351c75;">In 2003, Heiko Braak and colleagues published extensive research that analyzed brain tissue from 168 samples of cases diagnosed with <a href="https://neurology.cmesociety.com/call-for-abstracts" target="_blank">Parkinson's disease,</a> cases with indications of the disease and individuals without neurological disorders. The objective was to compare the lesions in the samples and establish a pattern of Parkinson's<a href="https://neurology.cmesociety.com/abstract-submission" target="_blank"> progression</a>. One of the key lesions in the disease is the toxic buildup of a protein called alpha-synuclein in affected neurons. They found in the patients studied the accumulation of alpha-synuclein in a part of the vagus nerve, which is responsible for intestinal functions. Braak suggested a new mechanism combining his observations with other reports of defective alpha-synuclein in the intestinal tract of <a href="https://neurology.cmesociety.com/abstract-submission" target="_blank">Parkinson's patients</a>. It was speculatively suggested that the disease was following a progression similar to that of a "pathogen" and that the entry route could be the intestine. Although this work continues to be a benchmark for Parkinson's research, many other studies have shown that not all patients follow the stages of progression suggested by Braak et al. There are reports of up to 50% of patients studied that do not agree with the pathological signs described in the Braak stage system (Kalaitzakis, 2008).<o:p></o:p></span></div>
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<span style="color: #351c75;">Currently an "<a href="https://neurology.cmesociety.com/abstract-submission" target="_blank">unknown pathogen</a>" is not the first line of research as the origin of the disease. Environmental factors that use the vagus nerve as a transport route have also been suggested as possible initiators or catalysts. But there are still questions about this mechanism of propagation of Parkinson's disease, such as Why is the distribution of alpha-synuclein accumulations so variable once they reach the brain of patients? o Why would alpha-synuclein begin to accumulate defectively in the intestine in the first place? Till the date,<o:p></o:p></span></div>
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<span style="color: #351c75;">2. The <a href="https://neurology.cmesociety.com/abstract-submission" target="_blank">intestinal flora</a> and its possible <a href="https://neurology.cmesociety.com/abstract-submission" target="_blank">role in the disease</a></span></h4>
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<span style="color: #351c75;">Different research groups have studied the changes in intestinal flora in patients with Parkinson's. For example, some groups have described a greater abundance of bacterial families in Parkinson's patients than in people without the disease. <o:p></o:p></span></div>
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<span style="color: #351c75;">Other groups have associated the presence of certain bacteria with worsening of symptoms in patients. Some groups began to observe that the intestinal flora of Parkinson's patients with <a href="https://neurology.cmesociety.com/call-for-abstracts/rehabilitation-process-in-neuromedicine" target="_blank">motor complications</a> has more abundance of some types of bacteria, compared with patients who do not develop those specific symptoms. It was also reported that patients with Parkinson's who suffer gastrointestinal infections caused by the bacterium <i>Helicobacter pylori</i> present more serious motor symptoms. Recently, a research group led by Sarkis Mazmanian showed that metabolites produced by certain bacteria can worsen the motor symptoms and brain pathology of model mice of this disease.<o:p></o:p></span></div>
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<span style="color: #351c75;">Changes in bacterial flora have also been associated with specific drugs that are used to treat patients (Scheperjans, 2015). However, it is still unclear if the prevalence of certain bacteria can influence the metabolism of drugs and affect the regulation of motor symptoms.<o:p></o:p></span></div>
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<span style="color: #351c75;">Although all these investigations present a relation between intestinal flora and Parkinson's disease, the evidence is very limited to issue conclusions about the relevance of treatments that involve the intestinal flora for the disease. These studies have not made clear whether changes in the intestinal flora are a cause or consequence of Parkinson's disease. Therefore, the relationship between certain types of bacteria in the intestinal flora and the processing of medications administered to patients should be properly investigated before proposing the intestinal flora as a target for treatment.<o:p></o:p></span></div>
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<span style="color: #351c75;">3. <a href="https://neurology.cmesociety.com/call-for-abstracts/neuromedicine" target="_blank">Inflammation</a>, key process for a new model</span></h4>
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<span style="color: #351c75;">In recent years, a model of disease progression that involves <a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-immunology" target="_blank">inflammation</a> in the intestine has become more important. This model tries to combine evidence of reports of patients with intestinal inflammation, associations of Parkinson's disease with other intestinal diseases and the implication of important agents for Parkinson's disease with <a href="https://neurology.cmesociety.com/call-for-abstracts/neuromedicine" target="_blank">immunological processes</a> in our body. A greater probability (28%) of developing Parkinson's disease was reported in a considerable number of patients with inflammatory bowel diseases. One of these diseases is Crohn's disease, an intestinal disorder related to Parkinson's disease due to a gene ( <i>LRRK2</i> ) associated with these two diseases, which has a role in the regulation of <a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-immunology" target="_blank">inflammatory processes.</a><o:p></o:p></span></div>
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<span style="color: #351c75;">Do you remember alpha-synuclein? now more studies relate it to processes of immune response and inflammation. Increased inflammatory activity may increase alpha-synuclein levels in the intestine and in the brain. It has also been observed that alpha-synuclein stimulates inflammatory responses by promoting a cycle that further complicates the disease and would help the spread to other organs and tissues.<o:p></o:p></span></div>
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<span style="color: #351c75;">The model now suggested indicates that an external factor could trigger an immune response of chronic inflammation, which, when not regulated by the organism, would affect the intestinal flora and the production of proteins such as alpha-synuclein. The accumulation of defective alpha-synuclein would spread from the intestine to the brain through the vagus nerve and from there it would affect different neurons, including those that produce dopamine, to give rise to Parkinson's disease.<o:p></o:p></span></div>
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<span style="color: #351c75;">Although this model combines Braak's observations with recent findings about the disease, it still does not conclude whether intestinal complications are a cause or consequence of the disease. It is known that the intestinal symptoms of the disease precede the motor, but this does not indicate that the cause of the disease is in the intestine. Nor does it explain why a proportion of patients do not present intestinal disorders, nor does it resolve the aforementioned inconsistencies of the Braak system. In addition, this new model does not exclude the possible existence of an external factor that would cause intestinal inflammation, so in this case the intestinal anomalies would not represent the true origin.<o:p></o:p></span></div>
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<span style="color: #351c75;">All these studies begin to give more indications of the different faults in the organism that occur in Parkinson's disease. As mentioned above, it is possible that Parkinson's disease has different origins, which explains the different symptoms and patterns of progression in each of the patients. This also agrees with the difficulties that exist to establish an effective treatment for this disease, since each patient develops differently.<o:p></o:p></span></div>
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<o:p><a href="https://neurology.cmesociety.com/abstract-submission" target="_blank"><span style="color: #351c75;"> Submit your Abstract </span></a></o:p></div>
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<span style="color: #351c75;">Chris Isaac</span></div>
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<span style="color: #351c75;">Neurology 2018 </span></div>
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<span style="color: #351c75;">July 4, 2018 by Melissa Leija Salazar<o:p></o:p></span></div>
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Anonymoushttp://www.blogger.com/profile/08717434777680943377noreply@blogger.com0tag:blogger.com,1999:blog-74280172020055059.post-36082977533181991172018-07-03T23:26:00.000-07:002018-07-04T23:18:34.665-07:00Neuro Cardiology | Neurology2018 | Brain-Heart | Neurology Conference 2018 <div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="color: #351c75;"><b><span style="font-family: "times new roman" , serif; font-size: 12.0pt;"><a href="https://neurology.cmesociety.com/" target="_blank">Neuro-cardiology</a></span></b><span style="font-family: "times new roman" , serif; font-size: 12.0pt;"> refers to the pathophysiological interplays of the <a href="https://neurology.cmesociety.com/call-for-abstracts/neurology" target="_blank">nervous</a> and cardiovascular systems. The constant communication between the heart and the brain have proved invaluable to interdisciplinary fields of<a href="https://neurology.cmesociety.com/call-for-abstracts/neurology" target="_blank"> <b>neurological</b></a> and cardiac diseases. <o:p></o:p></span></span></div>
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<span style="color: #351c75;">The interaction between heart and <a href="https://neurology.cmesociety.com/" target="_blank">brain </a>becomes increasingly important as the underlying mutual mechanisms become better understood. The speciality that deals with the brain-heart connection has become known as neurocardiology. </span></div>
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<a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEizSRE9Q7_17r_Kuo0YSCdDp4xf_p61yrAcX1DgxuLzJvKkO8M91YyD5NGLBwiiW6bd2ZvSd2Ju5fO6MI3gnAOpZuVhiwbOToCuh3S8EZFXsdWDysfesXqgwtEXLCBKblxvOS9Lol0ei80/s1600/fpsyg-05-01040-g009.jpg" imageanchor="1" style="clear: right; float: right; margin-bottom: 1em; margin-left: 1em;"><span style="color: #351c75;"><img border="0" data-original-height="479" data-original-width="397" height="320" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEizSRE9Q7_17r_Kuo0YSCdDp4xf_p61yrAcX1DgxuLzJvKkO8M91YyD5NGLBwiiW6bd2ZvSd2Ju5fO6MI3gnAOpZuVhiwbOToCuh3S8EZFXsdWDysfesXqgwtEXLCBKblxvOS9Lol0ei80/s320/fpsyg-05-01040-g009.jpg" width="265" /></span></a></div>
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<span style="color: #351c75;">Over the past years, there is increasing evidence about the brain-heart interaction with major potential implications for treatment of cardiovascular diseases. For instance, cerebrovascular accidents (CVAs) and transient ischaemic attacks (TIAs) are frequently caused by cardiac arrhythmias and/or congestive heart failure.</span></div>
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<span style="color: #351c75;">Even in the absence of manifest stroke, atrial fibrillation is a risk factor for <a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-psychiatry" target="_blank">cognitive impairment </a>and hippocampal atrophy. Therefore, cognition and measures of structural <a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-psychiatry" target="_blank">brain integrity</a> should be considered in the evaluation of novel treatments for atrial fibrillation. <o:p></o:p></span></div>
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<span style="color: #351c75;">There are complex and dynamic reflex <a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-psychiatry" target="_blank">control networks </a>between the heart and the brain, including cardiac and intrathoracic ganglia, <a href="https://neurology.cmesociety.com/call-for-abstracts/neurosurgery" target="_blank">spinal cord</a>, <a href="https://neurology.cmesociety.com/call-for-abstracts/neurosurgery" target="_blank">brainstem</a>, and central nucleus. Recent literature based on animal model and clinical trials indicates a close link between cardiac function and nervous systems. It is noteworthy that the autonomic nervous-based therapeutics has shown great potential in the management of atrial fibrillation, ventricular arrhythmia, and myocardial remodeling. However, the potential mechanisms of postoperative <a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-intensive-care-unit" target="_blank">brain injury</a> and cardiovascular changes, particularly heart rate variability and the presence of arrhythmias, are not understood. In this chapter, we will describe mechanisms of <a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-intensive-care-unit" target="_blank">brain damage</a> undergoing cardiac surgery and focus on the interaction between cardiovascular changes and damage to specific brain regions.<o:p></o:p></span></div>
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<span style="color: #351c75;">Improving our understanding of the mechanisms regulating postoperative brain injury and cardiovascular changes will aid in the development of appropriate therapeutic measures for cardiac surgery patients. Careful management of the operation period and favourable cardiopulmonary bypass conditions, as well as control of temperature, flow rate, pH, and hematocrit levels, can reduce the risk of cerebral infarction and thus avoid autonomic nerve damage and improve the prognosis of patients with cardiac surgery . Similarly, furthering our understanding of the brain-heart axis and how brain lesions result in dynamic changes in ECG and HRV is important for facilitating the treatment of clinical symptoms in patients with brain injury after cardiac surgery.<o:p></o:p></span></div>
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<span style="color: #351c75;">Submit your Abstracts : <a href="https://neurology.cmesociety.com/abstract-submission">https://neurology.cmesociety.com/abstract-submission</a> </span></div>
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Anonymoushttp://www.blogger.com/profile/08717434777680943377noreply@blogger.com2tag:blogger.com,1999:blog-74280172020055059.post-77923014908297461462018-07-03T22:22:00.002-07:002018-07-03T22:22:53.355-07:00Neurology 2018 | Functional Magnetic Resonance Imaging (fMRI) | Neurology Conference 2018 | Mental Imaginary | <div dir="ltr" style="text-align: left;" trbidi="on">
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<a href="https://neurology.cmesociety.com/" target="_blank">Neurological Basis</a> | <a href="https://neurology.cmesociety.com/call-for-abstracts/neurological-examination-imaging-radiology" target="_blank">Functional Magnetic Resonance Imaging (fMRI)</a> | Neurology Conference 2018 | Mental Imaginary </div>
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A team led by UNSW Associate Professor Joel Pearson has launched a crowd-funding campaign to raise money to carry out <a href="https://neurology.cmesociety.com/call-for-abstracts/neurological-examination-imaging-radiology" target="_blank">functional magnetic resonance imaging (fMRI) </a>studies to try and understand the neurological basis of<a href="https://neurology.cmesociety.com/call-for-abstracts/neurological-examination-imaging-radiology" target="_blank"> mental imagery.</a><o:p></o:p></div>
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People with and without congential aphantasia – which has only recently been recognised as a new condition – will participate. The findings could also have implications for common mental disorders such as schizophrenia and <a href="https://neurology.cmesociety.com/" target="_blank">Parkinson’s disease, </a>which are associated with disturbed mental imagery.<o:p></o:p></div>
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“Close your eyes and imagine a green apple floating in front of you,” says Associate Professor Pearson, of the School of <a href="https://neurology.cmesociety.com/" target="_blank">Psychology </a>at UNSW Science.<o:p></o:p></div>
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<i>“It may be that people with aphantasia are not able to activate these patterns enough to see mental images, or they may use a completely different network of brain activity to imagine.”<o:p></o:p></i></div>
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“The small number of people who have aphantasia are often very surprised to discover that most other people can easily do this.<o:p></o:p></div>
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“They say they have no visual experience at all. No matter how hard they try, they cannot picture an apple, or any other familiar object in their mind’s eye.”<o:p></o:p></div>
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Mental imagery is involved in many everyday tasks, such as remembering the past, navigating, and recognising faces, as well as in psychological treatments such as cognitive behaviour therapy.<br />
<br />However, little is known about the number of people with aphantasia, nor how it affects their lives, positively or negatively.<o:p></o:p></div>
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Some researchers have suggested people with aphantasia may be able to create mental images, but their problem is one of introspection, which means they cannot describe the images.<o:p></o:p></div>
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A recent study by Associate Professor Pearson and his UNSW colleague Dr Rebecca Keogh, however, suggests this is not the case and that people with the condition have no visual imagery.<o:p></o:p></div>
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“Current theories propose that when we imagine something, we try to reactivate the same pattern of activity in our brain as when we saw the image before,” says Dr Keogh.<o:p></o:p></div>
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“The better we are at this, the better our visual imagery is. It may be that people with <a href="https://neurology.cmesociety.com/abstract-submission" target="_blank">aphantasia </a>are not able to activate these patterns enough to see mental images, or they may use a completely different network of brain activity to imagine.”<o:p></o:p></div>
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The proposed<a href="https://neurology.cmesociety.com/call-for-abstracts" target="_blank"> fMRI</a> study will try to uncover any structural and functional differences in the brains of people with aphantasia.<o:p></o:p></div>
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“The research could help us enrich the inner lives of people with aphantasia, enhance the visual imagery of other people, as well as have an impact on a range of disorders and treatments,” says Associate Professor Pearson.<o:p></o:p></div>
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“This is the first step towards the possibility of giving aphantasics the experience of imagery.”<o:p></o:p></div>
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Source: UNSW<o:p></o:p></div>
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Anonymoushttp://www.blogger.com/profile/08717434777680943377noreply@blogger.com0tag:blogger.com,1999:blog-74280172020055059.post-84729097937261641672018-06-27T21:37:00.000-07:002018-06-27T21:37:43.530-07:00Neuroscience | Neurology Conference 2018 | Submit Your Abstracts | CME Conference <div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="color: #333333; font-family: "Times New Roman",serif; font-size: 12.0pt; line-height: 107%; mso-fareast-font-family: "Times New Roman"; mso-fareast-language: EN-IN;"><a href="https://neurology.cmesociety.com/" target="_blank">Scientists Discover How Brain Signals Travel to Drive Language Performance</a><o:p></o:p></span></div>
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<span style="color: blue;">Submit your Abstracts</span><span style="color: #cc0000;"> </span><a href="https://neurology.cmesociety.com/abstract-submission" target="_blank">here </a></div>
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<span style="color: blue;"><span style="font-family: "Times New Roman", serif; font-size: 12pt;">Effective verbal </span><a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-psychology" style="font-family: "Times New Roman", serif; font-size: 12pt;" target="_blank">communication</a><span style="font-family: "Times New Roman", serif; font-size: 12pt;"> depends on one’s ability to retrieve and select the appropriate words to convey an intended meaning. For many, this process is instinctive, but for someone who has suffered a stroke or another type of brain damage, communicating even the most basic message can be arduous.</span></span></div>
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<span style="font-family: "Times New Roman", serif; font-size: 12pt; line-height: 107%;"><span style="color: blue;">Scientists know that a <a href="https://neurology.cmesociety.com/call-for-abstracts/neuro-psychology" target="_blank">brain </a>region called the left inferior frontal gyrus (LIFG) is critical for language production and word processing. However, it remains unclear how exactly the LIFG interacts with the brain’s complex networks to facilitate controlled language performance — or how these interactions might go awry in a damaged brain.<o:p></o:p></span></span></div>
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<span style="font-family: "Times New Roman", serif; font-size: 12pt; line-height: 107%;"><span style="color: blue;">Using a <a href="https://neurology.cmesociety.com/call-for-abstracts/neurological-examination-imaging-radiology" target="_blank">magnetic brain stimulation technique</a> — the same method sometimes used to treat depressive symptoms — and network control theory, researchers at Drexel University and the University of Pennsylvania have taken a novel approach to understanding how networks in the brain interact to make word-choice decisions. Their results, published this month in the <a href="https://neurology.cmesociety.com/call-for-abstracts/neuroscience" target="_blank"><i>Journal of Neuroscience</i>,</a> pave the way for the treatment of aphasia and other language disorders.<o:p></o:p></span></span></div>
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<span style="font-family: "Times New Roman", serif; font-size: 12pt; line-height: 107%;"><span style="color: blue;">“Our ability to understand neural systems is fundamentally related to our ability to control them,” said <b>J</b>ohn Medaglia, PhD, an assistant professor of psychology at Drexel University and the study’s primary author. “This research provides direct evidence that how we choose the words we want to say in natural language is related to the capability of the brain to integrate and segregate activity across major networks.”<o:p></o:p></span></span></div>
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<span style="font-family: "Times New Roman", serif; font-size: 12pt; line-height: 107%;"><span style="color: blue;">“Network <a href="https://neurology.cmesociety.com/call-for-abstracts/neuroscience" target="_blank">neuroscience</a> provides computational methods to uncover structure in brain imaging data.”<o:p></o:p></span></span></div>
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<span style="font-family: "Times New Roman", serif; font-size: 12pt; line-height: 107%;"><span style="color: blue;">Medaglia, along with his colleague and study co-author Danielle Bassett, PhD, at the University of Pennsylvania, seek to map out the entire landscape of the brain and to uncover how stimulating one network might connect to or affect another depending on experiences — a new, emerging field of research called network <a href="https://neurology.cmesociety.com/call-for-abstracts/neurological-examination-imaging-radiology" target="_blank">neuroscience</a>.<o:p></o:p></span></span></div>
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<span style="font-family: "Times New Roman", serif; font-size: 12pt; line-height: 107%;"><span style="color: blue;">“<a href="https://neurology.cmesociety.com/call-for-abstracts/neurology" target="_blank">Network neuroscience</a> provides computational methods to uncover structure in brain imaging data. In turn, knowledge about this structure allows us to better understand how signals travel naturally across the brain’s highways, and also how stimulation can alter that travel in a way that supports better cognitive function,” Bassett said.<o:p></o:p></span></span></div>
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<span style="font-family: "Times New Roman", serif; font-size: 12pt; line-height: 107%;"><span style="color: blue;">To see how the LIFG brain region is involved with different neural networks depending on various language tasks, the research team used a technique called transcranial magnetic stimulation, or TMS, which uses an external magnetic field to induce currents in parts brain.<br />
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<span style="font-family: "Times New Roman", serif; font-size: 12pt; line-height: 107%;"><span style="color: blue;">Twenty-eight study subjects were asked to complete two different kinds of language tasks while the research team administered the noninvasive brain stimulation. In the first type of task, study participants completed open-ended sentences such as, “They left the dirty dishes in the…” and were instructed to say a single word that would appropriately complete it. In the second type of task, study participants were asked to name specific images or numerals presented to them.<o:p></o:p></span></span></div>
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<span style="font-family: "Times New Roman", serif; font-size: 12pt; line-height: 107%;"><span style="color: blue;">For each task, the researchers measured the participants’ response times and administered brain stimulation. After collecting the data, the researchers used mathematical formulas to study the controllability of the brain’s network systems. They were focused on how the language tasks affected two distinct network control features: modal controllability, which is the ability of a brain region to drive a network into “difficult to reach” states and boundary controllability, the theoretical ability of a brain region to guide distinct brain networks to communicate with each other.<o:p></o:p></span></span></div>
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<span style="color: blue;"><span style="font-family: "Times New Roman", serif; font-size: 12pt; line-height: 107%;">The researchers found that boundary controllability represented a process importa</span>nt<span style="font-family: "Times New Roman", serif; font-size: 12pt;"> for responding in the open-ended language tasks, when participants needed to retrieve and select a single word in the face of competing, alternative responses. By contrast, modal controllability was closely related to closed-ended language tasks. This suggests that the LIFG’s ability to integrate and segregate communication between brain networks may not play an important role when people are selecting a single, correct word, rather than choosing among several possibilities.</span></span></div>
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<span style="font-family: "Times New Roman", serif; font-size: 12pt; line-height: 107%;"><span style="color: blue;">Medaglia says his group was surprised to find this very clear distinction between how the brain responds to two similar language tasks.<o:p></o:p></span></span></div>
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<span style="font-family: "Times New Roman", serif; font-size: 12pt; line-height: 107%;"><span style="color: blue;">“It was also surprising to me that you could find this effect when studying the whole brain, whereas a lot of traditional views on language would have you focus on a much more specific area.”<o:p></o:p></span></span></div>
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<span style="font-family: "Times New Roman", serif; font-size: 12pt; line-height: 107%;"><span style="color: blue;">“I thought our results would be more muddied. There are debates about how unique these processes truly are, and now we have evidence that you can make a clear distinction between them,” Medaglia said. “It was also surprising to me that you could find this effect when studying the whole brain, whereas a lot of traditional views on language would have you focus on a much more specific area.”<o:p></o:p></span></span></div>
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<span style="font-family: "Times New Roman", serif; font-size: 12pt; line-height: 107%;"><span style="color: blue;">Next, the research team is using the same type of techniques in stroke patients to see if stimulating certain areas of the brain can help them to improve their speech.<o:p></o:p></span></span></div>
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<span style="font-family: "Times New Roman", serif; font-size: 12pt; line-height: 107%;"><span style="color: blue;">Study co-author <b>Roy Hamilton, MD, </b>a behavioral neurologist in the Perelman School of Medicine at the University of Pennsylvania, suggests that these findings may someday benefit patients with aphasia (acquired language loss due to stroke). For patients with aphasia, partial language recovery is often associated with the reorganization of the language system in the brain — language functions performed by damaged areas of the brain shift to new areas that had not previously been involved in language processing.<o:p></o:p></span></span></div>
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<span style="font-family: "Times New Roman", serif; font-size: 12pt; line-height: 107%;"><span style="color: blue;">“This study gives us new insight into the underlying properties of areas like the LIFG that enable the brain to process language,” Hamilton said. “But there are still questions we’re looking to answer. For example, what determines which new areas of the brain will be recruited for language processing? What properties make them good candidates? With further research, we can begin to uncover which areas of the brain are likely to be utilized if there’s an injury to the language system. This approach may provide exciting new targets for treatment with focal therapies, including <a href="https://neurology.cmesociety.com/call-for-abstracts/neuroscience" target="_blank">neuromodulation</a></span><span style="color: #333333;"><o:p></o:p></span></span></div>
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Anonymoushttp://www.blogger.com/profile/08717434777680943377noreply@blogger.com1tag:blogger.com,1999:blog-74280172020055059.post-47132854999971587432018-06-25T23:55:00.000-07:002018-06-25T23:55:04.613-07:00Neurology Conference 2018 | Human Brain | Neurology 2018 <div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="background-color: white; color: #333333; font-family: Roboto; font-size: 16px;">A <a href="https://neurology.cmesociety.com/call-for-abstracts" target="_blank">human brain </a>is the largest, the developed structure in the anatomy of human beings and other well-organized organisms. The brain is made up of about 100 billion neurons and it weighs about 1300g or 3lbs.</span></div>
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The brain is called the <a href="https://neurology.cmesociety.com/abstract-submission" target="_blank">Central Nervous System </a>as it performs our body’s decision and is the communication center for organs and activities. The Peripheral Nervous System and the spinal cord is composed of nerves. The daily activities starting from breathing, blinking of our eyes to reflex action and to memorize the facts are altogether controlled by these two systems –</div>
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<li style="border: 0px; box-sizing: border-box; font-family: inherit; font-style: inherit; font-weight: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><a href="https://neurology.cmesociety.com/abstract-submission" target="_blank">The central nervous system – CNS</a></li>
<li style="border: 0px; box-sizing: border-box; font-family: inherit; font-style: inherit; font-weight: inherit; margin: 0px; padding: 0px; vertical-align: baseline;"><a href="https://neurology.cmesociety.com/" target="_blank">The Peripheral Nervous System – PNS.</a></li>
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The brain is the part of the central nervous system present in the head and is protected by the skull, both laterally and dorsally. Cranium, a bony structure is called as the house for the brain which is located within the skull. It is also known as the centralized command for the nervous system, as brain receives information from the sensory organs and sends output through the muscles.</div>
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The brain is made up of different chambers and compartments for various functions. A human brain works continuously day and night by sending instructions to different organs of our body and function as per the requirements.</div>
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Submit your abstracts <a href="https://neurology.cmesociety.com/abstract-submission" target="_blank">here</a></div>
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Anonymoushttp://www.blogger.com/profile/08717434777680943377noreply@blogger.com0tag:blogger.com,1999:blog-74280172020055059.post-43709766724649805792018-06-21T05:49:00.000-07:002018-06-25T05:34:25.380-07:00Neurology Conference 2018 | Abstracts Invited | CME | Berlin | Germany <div dir="ltr" style="text-align: left;" trbidi="on">
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<b><i><span style="color: blue; font-size: 16.0pt; line-height: 107%;"><a href="https://neurology.cmesociety.com/" target="_blank">Exploring the Sources for A Better Neurocare And Healthcare Through Neurology 2018<o:p></o:p></a></span></i></b></div>
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<b><i><span style="color: blue; font-size: 16.0pt; line-height: 107%;">(CME Accredited Neurology Conference)<o:p></o:p></span></i></b></div>
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<b><i><span style="color: blue; font-size: 12.0pt; line-height: 107%;">4<sup>th</sup> International Conference on Neurology and Healthcare<o:p></o:p></span></i></b></div>
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<b><i><span style="font-size: 12.0pt; line-height: 107%;"><span style="color: blue;">September 17-18, 2018 Berlin, Germany</span><o:p></o:p></span></i></b></div>
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<b><i><span style="color: blue;">The <a href="https://neurology.cmesociety.com/abstract-submission" target="_blank">Conference</a> serves as a platform to discuss the growing trends in <a href="https://neurology.cmesociety.com/abstract-submission" target="_blank">Neurology</a> and Neuroscience which could unleash the buckles of many unrecognised research works which are in a developing phase. The trend towards the developing strategies of <a href="https://neurology.cmesociety.com/call-for-abstracts" target="_blank">surgical methods </a>also widens the opportunity for the researchers and scientists to establish their own signature in the field, thereby witnessing a tremendous change in the work field. </span><o:p></o:p></i></b></div>
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<b><i><span lang="EN-US">Submit your abstracts at <a href="https://neurology.cmesociety.com/abstract-submission">https://neurology.cmesociety.com/abstract-submission</a></span> </i></b><b><i><span lang="EN-US"><o:p></o:p></span></i></b></div>
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<span style="color: #0c343d;">Pulsus Conferences hosts the<b> <a href="https://neurology.cmesociety.com/" target="_blank">4th International Conference on Neurology and Healthcare</a> (CME ACCREDITED)</b> which outsources the new research standards in neurocare and advanced healthcare , providing the most integrated approach in academic and research part of healthcare studies. Neurology 2018 will be unique in the series of conferences which will<span lang="EN-US"> provide interactive sessions regarding Neurocare and quality aspects followed in healthcare industries along with recent advances in the field of neuro robotics. It also provides an opportunity to showcase your research works and innovative works in front of the world for the global recognition. <b><a href="https://neurology.cmesociety.com/abstract-submission" target="_blank">The event is held at Berlin from September 17-18 ,2018. CME Credits are Awarded for the Conference </a><o:p></o:p></b></span></span></div>
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<span lang="EN-US" style="color: #0c343d;">Neurology 2018 will witness the gathering of International blend of people from neurological field, pharmaceutical, biotech & medical devices companies, business entrepreneurs, neurology consultants, R&D heads and decision makers from healthcare, contract research, clinical trials, leading universities and research institutions making it the largest endeavor from Pulsus Conferences.<o:p></o:p></span></div>
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<span style="color: #073763;"><span lang="EN-US" style="font-family: "times new roman" , serif; mso-ansi-language: EN-US; mso-bidi-font-weight: bold;">I</span><span style="font-family: "times new roman" , serif;">f you would like to know more information about this conference, <o:p></o:p></span></span></div>
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<span style="color: #073763; font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">Contact:<o:p></o:p></span></div>
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<span style="color: #073763; font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">Chris Isaac<o:p></o:p></span></div>
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<span lang="EN-US" style="color: #073763; font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;">Program Manager | Neurology 2018<o:p></o:p></span></div>
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<span lang="EN-US" style="font-family: "times new roman" , serif; font-size: 14.0pt; line-height: 107%;"><a href="mailto:neurology@pulsusevents.org"><span style="color: #073763;">neurology@pulsusevents.org</span></a> <o:p></o:p></span></div>
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Anonymoushttp://www.blogger.com/profile/08717434777680943377noreply@blogger.com0tag:blogger.com,1999:blog-74280172020055059.post-56831907544195862962018-06-21T05:12:00.001-07:002018-06-25T05:28:21.293-07:00Neurology Conference 2018 | Impulse control | Parkinson's Disease | Abstract Submission <div dir="ltr" style="text-align: left;" trbidi="on">
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Impulse control disorders in Parkinson’s patients may be higher than thought- Neurology2018</h1>
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Neurology 2018 - <a href="https://neurology.cmesociety.com/abstract-submission" target="_blank">Submit Your Abstracts </a></h3>
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<a href="https://neurology.cmesociety.com/" target="_blank">4th International Conference on Neurology and Healthcare </a></div>
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Nearly half of patients with <a href="https://neurology.cmesociety.com/call-for-abstracts" target="_blank">Parkinson’s disease</a> who were taking dopamine agonist treatment experienced impulse control disorders over a follow-up of 5 years, according to recently published results of a longitudinal study.</div>
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The 5-year cumulative incidence of impulse control disorders was approximately 45% in the study, which included 411 patients with a high prevalence of dopamine agonist use and disease duration of 5 years or less at baseline.</div>
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There was a strong association between dopamine agonist use and impulse control disorders in the study, which was conducted by <span class="Hyperlink" style="box-sizing: border-box;">Jean-Christophe Corvol, MD</span>, of Publique Hôpitaux de Paris and his co-investigators.</div>
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<a href="https://neurology.cmesociety.com/call-for-abstracts" target="_blank">Impulse disorders </a>increased in incidence with both duration and dose of dopamine agonists and resolved progressively after discontinuation of those agents, the investigators reported online June 20 in <span class="Hyperlink" style="box-sizing: border-box;">Neurology</span>. The investigators used item 1.6 of part I of the Movement Disorder Society Unified Parkinson’s Disease Rating Scale to determine the presence of an impulse control disorder.</div>
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“Given the high cumulative incidence of impulse control disorders in patients with Parkinson’s disease, these adverse effects should be carefully monitored in patients ever treated with dopamine agonists,” Dr. Corvol and his coauthors wrote.</div>
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The results came from the ongoing <a href="https://neurology.cmesociety.com/call-for-abstracts" target="_blank">Drug Interaction </a>With Genes in Parkinson’s Disease (DIGPD) study, a longitudinal cohort study including Parkinson’s disease patients consecutively recruited between 2009 and 2013 at eight French hospitals. All patients had no more than 5 years of disease duration at recruitment, and follow-up included annual evaluations by movement disorder specialists.</div>
<article about="/clinicalneurologynews/article/113904/movement-disorders/experts-offer-tips-anxiety-depression-and" class="related-callout node node-article node-promoted node-view-mode-related clearfix" id="node-113904" role="article" style="border-bottom: 1px solid rgb(204, 204, 204); border-top: 1px solid rgb(204, 204, 204); box-sizing: border-box; line-height: 1.2; margin: 25px 0px; padding: 10px;" typeof="sioc:Item foaf:Document"><div class="related-callout__header" style="box-sizing: border-box; font-family: adelle-sans, "Helvetica Neue", Helvetica, Arial, sans-serif; font-size: 12px; font-weight: 700; text-transform: uppercase;">
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At baseline, the majority of patients (302, or 73.5%) had taken dopamine agonists within the past 12 months.</div>
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Over the course of 5 years, the prevalence of impulse control disorders increased from 19.7% at baseline to 32.8%, Dr. Corvol and his colleagues reported.</div>
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Among 306 patients with no impulse control disorders at baseline, 94 developed one, for a 5-year cumulative incidence of 46.1%, they added. Only 4 of the 94 new cases occurred in patients who never used dopamine agonists.</div>
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Dopamine agonist use in the previous 12 months was associated with a 2.23-fold higher prevalence of impulse control disorders (<em style="box-sizing: border-box;">P</em> less than .001), with prevalence increasing along with average daily dose and cumulative dose duration over that time period, according to the investigators.</div>
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These findings suggests tools are needed to screen for impulse control disorders and identify high-risk patients, they said.</div>
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“Further studies are needed to understand the mechanisms involved in the relation between [dopamine agonists] and [impulse control disorders], in particular the role of apathy, anxiety, and depression,” they added.</div>
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<span style="color: #ffd966;">Source https://www.mdedge.com/clinicalneurologynews/article/168551/movement-disorders/impulse-control-disorders-parkinsons </span></div>
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Anonymoushttp://www.blogger.com/profile/08717434777680943377noreply@blogger.com0tag:blogger.com,1999:blog-74280172020055059.post-67724617334105373072018-06-13T05:26:00.004-07:002018-06-25T05:28:58.346-07:00Neurosurgery | Ancient Methods | Trepanation | Advanced ? | Neurology 2018<div dir="ltr" style="text-align: left;" trbidi="on">
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<a href="https://neurology.cmesociety.com/call-for-abstracts" target="_blank">Skull-drilling: The ancient roots of modern neurosurgery </a></h3>
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<header style="border-bottom-color: initial; border-bottom-style: initial; border-image: initial; border-left-color: initial; border-left-style: initial; border-right-color: initial; border-right-style: initial; border-top-color: rgb(229, 229, 229); border-top-style: solid; border-width: 1px 0px 0px; box-sizing: border-box; line-height: 36px; margin: 0px 0px 20px -1px; padding: 30px 0px 0px;">Over the years, archaeologists across the world have unearthed many ancient and medieval skeletons with mysterious holes in their skulls. It turned out that these holes were evidence of trepanation, an "ancestor" of modern brain surgery.</header><br />
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</span><span style="box-sizing: border-box; display: block; line-height: 18px; margin: 0px; padding: 10px 0px 0px;">Ancient Peruvians may have been better at handling skull perforation procedures than their modern-day counterparts.</span></div>
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Evidence of holes being drilled into the skull for medical purposes, or "trepanation," has been traced back to the Neolithic period — about 4000 B.C. — and it might have been practiced even earlier.</div>
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When it comes to the reasons why <a href="https://neurology.cmesociety.com/call-for-abstracts" target="_blank">trepanation</a> was practiced at all, opinions differ.</div>
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The operation may have been performed for various reasons across civilizations and eras.</div>
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Some of the trepanations may have been done for ritualistic purposes, but many others were probably performed to heal.</div>
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In a medical context, research has shown that trepanation was likely used to treat various types of head injuries and to relieve intracranial pressure.</div>
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Fascinatingly, the most cases of ancient trepanation have been found in Peru, where it was also also seen to have the highest survival rate.</div>
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A new study, in fact, shows that trepanation performed in the Incan period (early 15th–early 16th century) had higher survival rates than even modern trepanation procedures, such as those that were performed during the American Civil War (1861–1865) on soldiers who had suffered head trauma.</div>
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Dr. David S. Kushner, a clinical professor of physical medicine and rehabilitation at the University of Miami Miller School of Medicine in Florida, alongside world expert on Peruvian trepanantion John W. Verano and his former graduate student Anne R. Titelbaum, explain — in an article that is now published in the <em style="box-sizing: border-box;">World Neurosurgery</em> journal — that trepanation was surprisingly well developed in the Inca Empire.</div>
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"There are still many unknowns about the procedure and the individuals on whom trepanation was performed, but the outcomes during the Civil War were dismal compared to Incan times," says Dr. Kushner.</div>
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Dr. Kushner also believes that the Peruvians may have used something akin to anesthetic to make the procedure more bearable, and his first guess is coca leaves — which have been used for medicinal purposes by Andean populations for centuries.At the same time, he admits, "We do not know how the ancient Peruvians prevented infection, but it seems that they did a good job of it."</div>
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<span style="box-sizing: border-box; font-weight: 700;">"[We still do not] know what they used as [anesthetic], but since there were so many [cranial surgeries] they must have used something — possibly coca leaves," Dr. Kushner surmises, though he concedes that other substances may also have been employed.</span></div>
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The fact that the ancient Peruvians were clearly doing something well when it came to trepanation is supported by the evidence of over 800 prehistoric skulls bearing between one and seven precision holes.</div>
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All of these skulls were discovered along the coasts or in the Andean regions of Peru, with the earliest skulls dated as early as 400 B.C.</div>
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<span style="font-family: inherit;">Very high survival rates for ancient patients</span></div>
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Combined evidence — detailed by John Verano and colleagues in a book published 2 years ago, <em style="box-sizing: border-box;">Holes in the Head: The Art and Archaeology of Trepanation in Ancient Peru</em> — suggests that the ancient Peruvians had spent many a decade perfecting their trepanation knowledge and skills.</div>
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At first, in around 400–200 B.C., the survival rates following a trepanation weren't all that high, and about half of the patients did not survive, the researchers argue. The team was able to assess the outcomes by looking at how much — if at all — the bone surrounding the trepanation holes had healed after the procedure.</div>
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Where no healing seemed to have occurred, the team thought it safe to conclude that the patient had either survived for a short period of time or had died during the procedure.</div>
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When, to the contrary, the bone showed extensive remodeling, the researchers took it as a sign that the person operated upon had lived to tell the tale.</div>
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<span style="box-sizing: border-box; font-weight: 700;">Dr. Kushner and team found that, based on these signs, in 1000–1400 A.D., trepanation patients saw very high survival rates, of up to 91 percent in some cases. During the Incan period, this was 75–83 percent, on average.</span></div>
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This, the researchers explain in their paper, is due to ever-improving techniques and knowledge that the Peruvians acquired over time.</div>
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One such important advance was understanding that they should be careful not to penetrate the dura mater, or the protective layer found just under the skull, which protects the brain.</div>
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"Over time," says Dr. Kushner, "from the earliest to the latest, they learned which techniques were better, and less likely to perforate the dura." He continues, "They seemed to understand head anatomy and purposefully avoided the areas where there would be more bleeding."</div>
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Based on the evidence offered by the human remains uncovered in Peru, the researchers saw that other advances in trepanation practice also occurred.</div>
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Dr. Kushner goes on to explain, "[The ancient Peruvians] also realized that larger-sized trepanations were less likely to be as successful as smaller ones. Physical evidence definitely shows that these ancient surgeons refined the procedure over time."</div>
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He calls this ancient civilization's progress when it came to this risky procedure "truly remarkable."</div>
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It is these and similar practices that — directly or indirectly — have shaped modern neurosurgery, which has a high rate of positive outcomes.</div>
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<span style="box-sizing: border-box; font-weight: 700;">"Today, neurosurgical mortality rates are very, very low; there is always a risk but the likelihood of a good outcome is very high. And just like in ancient Peru, we continue to advance our neurosurgical techniques, our skills, our tools, and our knowledge," says Dr. Kushner.</span></div>
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Anonymoushttp://www.blogger.com/profile/08717434777680943377noreply@blogger.com0tag:blogger.com,1999:blog-74280172020055059.post-58907249542225388452018-06-08T23:24:00.001-07:002018-06-25T05:29:40.694-07:00Abstracts Invited | Deep brain stimulation | Neurology 2018 <div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="font-size: large;">Deep brain stimulation | Neurology 2018</span></h2>
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<span style="font-size: large;"> </span>https://neurology.cmesociety.com/ </div>
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<b><a href="https://neurology.cmesociety.com/call-for-abstracts" target="_blank">Deep brain stimulation</a> </b>(DBS) is a surgical procedure used to treat several disabling neurological symptoms—most commonly the debilitating motor symptoms of Parkinson’s disease (PD), such as tremor, rigidity, stiffness, slowed movement, and walking problems. The procedure is also used to treat essential tremor and dystonia. At present, the procedure is used only for individuals whose symptoms cannot be adequately controlled with medications. However, only individuals who improve to some degree after taking medication for Parkinson’s benefit from DBS. A variety of conditions may mimic PD but do not respond to medications or DBS. DBS uses a surgically implanted, battery-operated medical device called an implantable pulse generator (IPG) - similar to a heart pacemaker and approximately the size of a stopwatch to - deliver electrical stimulation to specific areas in the brain that control movement, thus blocking the abnormal nerve signals that cause PD symptoms.</div>
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Before the procedure, a <a href="https://neurology.cmesociety.com/call-for-abstracts" target="_blank">neurosurgeon</a> uses <a href="https://neurology.cmesociety.com/call-for-abstracts" target="_blank">magnetic resonance imaging</a> (MRI) or computed tomography (CT) scanning to identify and locate the exact target within the brain for surgical intervention. Some surgeons may use microelectrode recording - which involves a small wire that monitors the activity of nerve cells in the target area - to more specifically identify the precise brain area that will be stimulated. Generally, these areas are the thalamus, subthalamic nucleus, and globus pallidus. There is a low chance that placement of the stimulator may cause bleeding or infection in the brain.</div>
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The DBS system consists of three components: the lead, the extension, and the IPG. The lead (also called an electrode)—a thin, insulated wire—is inserted through a small opening in the skull and implanted in the brain. The tip of the electrode is positioned within the specific brain area. </div>
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The extension is an insulated wire that is passed under the skin of the head, neck, and shoulder, connecting the lead to the implantable pulse generator. The IPG (the "battery pack") is the third component and is usually implanted under the skin near the collarbone. In some cases it may be implanted lower in the chest or under the skin over the abdomen.</div>
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Once the system is in place, electrical impulses are sent from the IPG up along the extension wire and the lead and into the brain. These impulses block abnormal electrical signals and alleviate PD motor symptoms.<br />
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<a href="https://neurology.cmesociety.com/call-for-abstracts" target="_blank">Treatment</a><div class="separator" style="clear: both; text-align: center;">
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<span style="background-color: white; font-family: "source sans pro" , sans-serif;">Unlike previous surgeries for PD, DBS involves minimal permanent surgical changes to the brain. Instead, the procedure uses electrical stimulation to regulate electrical signals in neural circuits to and from identified areas in the brain to improve PD symptoms. Thus, if DBS causes unwanted side effects or newer, more promising treatments develop in the future, the implantable pulse generator can be removed, and the DBS procedure can be halted. Also, stimulation from the IPG is easily adjustable—without further surgery—if the person’s condition changes. Some people describe the pulse generator adjustments as "programming."</span><br />
<span style="background-color: white; font-family: "source sans pro" , sans-serif;"><br /></span> <span style="background-color: white; font-family: "source sans pro" , sans-serif;"><br /></span> <span style="background-color: white; font-family: "source sans pro" , sans-serif;">Although most individuals still need to take medication after undergoing DBS, many people with Parkinson’s disease experience considerable reduction of their motor symptoms and are able to reduce their medications. The amount of reduction varies but can be considerably reduced in most individuals, and can lead to a significant improvement in side effects such as dyskinesias (involuntary movements caused by long-term use of levodopa). In some cases, the stimulation itself can suppress dyskinesias without a reduction in medication. DBS does not improve cognitive symptoms in PD and indeed may worsen them, so it is not generally used if there are signs of dementia. DBS changes the brain firing pattern but does not slow the progression of the neurodegeneration.</span></div>
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Anonymoushttp://www.blogger.com/profile/08717434777680943377noreply@blogger.com1tag:blogger.com,1999:blog-74280172020055059.post-67028141258593013342018-06-08T05:59:00.002-07:002018-06-25T05:30:09.050-07:00Attractions In Berlin | Enjoy your conference | September Season <div dir="ltr" style="text-align: left;" trbidi="on">
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<span style="letter-spacing: -0.1pt; line-height: 120%;"><span style="font-size: x-large;"><a href="https://neurology.cmesociety.com/venue-hospitality" target="_blank">About Berlin</a></span></span></h2>
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<span style="font-weight: normal;"><span style="font-family: "calibri" , sans-serif; line-height: 107%;">Berlin </span>is the capital<span style="font-family: "calibri" , sans-serif; line-height: 107%;"> and the largest city located in northeastern part of <a href="https://neurology.cmesociety.com/" target="_blank">Germany </a>on the banks of rivers spree and have. Berlin serves with a temperate seasonal climate and one-third of </span><span lang="EN-US" style="font-family: "calibri" , sans-serif; line-height: 107%;">city's area is composed of forests, parks, gardens, rivers, canals and lakes</span>. Its a city of culture, politics, media and science and also serves as a continental hub for air and rail traffic and has essential public transportation network. Berlin was named as the city<span style="font-family: "simsun"; line-height: 107%;"></span><span style="font-family: "calibri" , sans-serif; line-height: 107%;"> of design</span><span style="font-family: "simsun"; line-height: 107%;">’</span><span style="font-family: "calibri" , sans-serif; line-height: 107%;"> UNESCO in 2005. </span><span lang="EN-US" style="font-family: "calibri" , sans-serif; line-height: 107%;">Berlin's nightlife has been celebrated as one of the most diverse and vibrant of its kind.</span><span style="font-family: "calibri" , sans-serif; line-height: 107%;"> German is the official language spoken in Berlin. </span><span lang="EN-US" style="font-family: "calibri" , sans-serif; line-height: 107%;">The</span><span lang="EN-US" style="font-family: "calibri" , sans-serif; line-height: 107%;"> </span></span><span lang="EN-US" style="font-family: "calibri" , sans-serif; line-height: 107%;"><span style="font-weight: normal;">most-commonly-spoken foreign languages in Berlin are Turkish, English, Russian, Arabic, Polish, Kurdish, Serbo-Croatian, Italian, Vietnamese, and French.</span><span style="font-size: 11pt;"><o:p></o:p></span></span></h4>
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<b><span style="font-family: "calibri" , sans-serif; line-height: 107%;"><span style="font-size: x-large;"><a href="https://neurology.cmesociety.com/venue-hospitality" target="_blank">Tourist attractions:</a></span></span></b></div>
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<b><a href="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjyfw_UneQlS27ltUGQ-hauh0zbHgiRRMHC6pMocJeb3Xap-43uzVFfrCgnvfx-Vuxjzv_lt5THquJHkRfZ0E7Z_y2ZM0LVZ_mURyJXSKSjh-OBxPMzCAQRY1Am8g7_ITBaPAbH6mfshWg/s1600/berlin_8_1115_oly_246_marcus_bredt.jpg" imageanchor="1" style="clear: left; float: left; margin-bottom: 1em; margin-right: 1em;"><img border="0" data-original-height="966" data-original-width="1600" height="193" src="https://blogger.googleusercontent.com/img/b/R29vZ2xl/AVvXsEjyfw_UneQlS27ltUGQ-hauh0zbHgiRRMHC6pMocJeb3Xap-43uzVFfrCgnvfx-Vuxjzv_lt5THquJHkRfZ0E7Z_y2ZM0LVZ_mURyJXSKSjh-OBxPMzCAQRY1Am8g7_ITBaPAbH6mfshWg/s320/berlin_8_1115_oly_246_marcus_bredt.jpg" width="320" /></a></b></div>
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<span style="font-family: "calibri" , sans-serif; line-height: 107%;">Being a tourist attraction city Berlin has the third place among most visited city in the European Union. Munich and Hamburg are the most visited places. Brandenburg Gate is an iconic landmark of Berlin which stands as a symbol of European history and of unity and peace.</span><span lang="EN-US" style="font-family: "calibri" , sans-serif; line-height: 107%;"> The <span class="MsoHyperlink"><span style="color: black; text-decoration-line: none;">East Side Gallery</span></span> is an open-air exhibition of art painted directly on the last existing portions of the Berlin Wall. It is the largest remaining evidence of the city's historical division. The <span class="MsoHyperlink"><span style="color: black; text-decoration-line: none;">Gendarmenmarkt</span></span> is a <span class="MsoHyperlink"><span style="color: black; text-decoration-line: none;">neoclassical</span></span> square in Berlin, the name of which derives from the headquarters of the famous Gens d'armes regiment located here in the 18th century. It is bordered by two similarly designed cathedrals, the <span class="MsoHyperlink"><span style="color: black; text-decoration-line: none;">Franz</span><span style="color: black; font-family: "times new roman" , serif; text-decoration-line: none;">ö</span><span style="color: black; text-decoration-line: none;">sischer Dom</span></span> with its observation platform and the <span class="MsoHyperlink"><span style="color: black; text-decoration-line: none;">Deutscher Dom</span></span>. The Konzerthaus (Concert Hall), home of the Berlin Symphony Orchestra, stands between the two cathedrals.</span><span style="font-family: "calibri" , sans-serif; line-height: 107%;"> Apart from this Berlin is famous for its cuisine and stay.</span><span lang="EN-US" style="font-family: "calibri" , sans-serif; font-size: 11pt; line-height: 107%;"><o:p></o:p></span></div>
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<b><span style="font-family: "times new roman" , serif; font-size: 12pt; line-height: 17.12px;">Neuroscience Research Institutions in Berlin<o:p></o:p></span></b></div>
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<span style="font-family: "wingdings"; font-size: 12pt; line-height: 17.12px;">l<span style="font-family: "times new roman"; font-size: 7pt; font-stretch: normal; line-height: normal;"> </span></span><span style="font-family: "times new roman" , serif; font-size: 12pt; line-height: 17.12px;">Institute for Theoretical Biology<o:p></o:p></span></div>
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<span style="font-family: "wingdings"; font-size: 12pt; line-height: 17.12px;">l<span style="font-family: "times new roman"; font-size: 7pt; font-stretch: normal; line-height: normal;"> </span></span><span style="font-family: "times new roman" , serif; font-size: 12pt; line-height: 17.12px;">Max Delbrück Center for Molecular Medicine <o:p></o:p></span></div>
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<span style="font-family: "wingdings"; font-size: 12pt; line-height: 17.12px;">l<span style="font-family: "times new roman"; font-size: 7pt; font-stretch: normal; line-height: normal;"> </span></span><span style="font-family: "times new roman" , serif; font-size: 12pt; line-height: 17.12px;">Cluster of Excellence "Neurocure"<o:p></o:p></span></div>
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<span style="font-family: "wingdings"; font-size: 12pt; line-height: 17.12px;">l<span style="font-family: "times new roman"; font-size: 7pt; font-stretch: normal; line-height: normal;"> </span></span><span style="font-family: "times new roman" , serif; font-size: 12pt; line-height: 17.12px;">Leibniz Institute for Molecular Pharmacology <o:p></o:p></span></div>
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<span style="font-family: "wingdings"; font-size: 12pt; line-height: 17.12px;">l<span style="font-family: "times new roman"; font-size: 7pt; font-stretch: normal; line-height: normal;"> </span></span><span style="font-family: "times new roman" , serif; font-size: 12pt; line-height: 17.12px;">Bernstein Center for Computational Neuroscience <o:p></o:p></span></div>
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<span style="font-family: "wingdings"; font-size: 12pt; line-height: 17.12px;">l<span style="font-family: "times new roman"; font-size: 7pt; font-stretch: normal; line-height: normal;"> </span></span><span style="font-family: "times new roman" , serif; font-size: 12pt; line-height: 17.12px;">Center for Stroke Research Berlin (CSB) <o:p></o:p></span></div>
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<span style="font-family: "wingdings"; font-size: 12pt; line-height: 17.12px;">l<span style="font-family: "times new roman"; font-size: 7pt; font-stretch: normal; line-height: normal;"> </span></span><span style="font-family: "times new roman" , serif; font-size: 12pt; line-height: 17.12px;">Berlin School of Mind and Brain<o:p></o:p></span></div>
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<span style="font-family: "wingdings"; font-size: 12pt; line-height: 17.12px;">l<span style="font-family: "times new roman"; font-size: 7pt; font-stretch: normal; line-height: normal;"> </span></span><span style="font-family: "times new roman" , serif; font-size: 12pt; line-height: 17.12px;">Berlin Neuro imaging Center<o:p></o:p></span></div>
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