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Deep brain stimulation (DBS) is an effective surgical treatment for movement disorders. Although stimulation sites for movement disorders such as Parkinson's disease are established, the therapeutic mechanisms of DBS remain controversial. Recent research suggests that specific white‐matter tract and circuit activation mediates symptom relief. To investigate these questions, we have developed a patient‐specific open‐source software pipeline called ‘DBSproc’ for (1) localizing DBS electrodes and contacts from postoperative CT images, (2) processing structural and diffusion MRI data, (3) registering all images to a common space, (4) estimating DBS activation volume from patient‐specific voltage and impedance, and (5) understanding the DBS contact‐brain connectivity through probabilistic tractography. In this paper, we explain our methodology and provide validation with anatomical and tractographic data. This method can be used to help investigate mechanisms of action of DBS, inform surgical and clinical assessments, and define new therapeutic targets. Hum Brain Mapp 37:422–433, 2016. Published 2015. This article is a U.S. Government work and is in the public domain in the USA.  相似文献   
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Background

The incidence of cerebral infarction and poor outcome in patients with aneurysmal subarachnoid hemorrhage (aSAH) is reduced by oral nimodipine but acute effects of the drug may include a significant decrease in mean arterial blood pressure (MAP). A dose reduction or discontinuation of the drug is recommended if recurrent MAP drops occur. The aim of our study was to evaluate the frequency and clinical significance of nimodipine dose modifications in patients suffering from aSAH.

Methods

270 patients were included in our retrospective analysis of consecutively collected data of patients suffering from aSAH. The local treatment protocol was in accordance to national and international guidelines. Nimodipine was intended to be applied orally with a dosage of 60 mg every 4 h.

Results

Only 43.6 % of patients eligible for vasospasm prophylaxis with nimodipine received the full daily dose of 60 mg every 4 h. In 28.6 %, the dose had to be reduced by 50 % due to a significant reduction in blood pressure after administration and/or high dose of catecholamines. In 27.7 % of patients, oral administration of the drug was discontinued for the same reason. Dose reduction and discontinuation occurred with a significantly higher frequency in patients in poor clinical condition. Application of the full nimodipine dosage decreased the risk of unfavorable clinical outcome in multivariate analysis (OR 0.895, p = 0.029).

Conclusions

Our results show that dose reduction or discontinuation of nimodipine due to changes in MAP occur frequently in clinical routine and may be associated with unfavorable clinical outcome.
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Cocaine's enhancement of dopamine signaling is crucial for its rewarding effects but its serotonergic effects are also relevant. Here we examined the role of the protein p11, which recruits serotonin 5HT1B and 5HT4 receptors to the cell surface, in cocaine reward. For this purpose we tested wild‐type (WT) and p11 knockout (KO) male and female mice for cocaine conditioned place preference (CPP) and its cocaine‐induced reinstatement at different abstinence times, after 8 days of extinction and 28 days of being home‐caged. All mice showed significant cocaine CPP. Among males, p11KO showed lower CPP than WT; this difference was also evident after 28 days of home‐cage abstinence. In contrast, in females there were no CPP differences between p11KO and WT mice at any time point tested. Cocaine priming after the 28‐day home‐cage abstinence period also resulted in lower cocaine conditioned motor activity in both male and female p11KO mice. These results suggest that cocaine CPP and its persistence during extinction and reinstatement are modulated in a sex‐differentiated manner by p11. The lack of protein p11 confers protection from CPP on male, but not female mice, immediately after cocaine conditioning as well as after prolonged abstinence, but not after short‐term withdrawal. Synapse 70:293–301, 2016. © 2016 Wiley Periodicals, Inc.  相似文献   
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New-onset refractory status epilepticus (NORSE) is a rare, potentially devastating condition that occurs abruptly in previously healthy patients of any age but most commonly in children and young adults. It has an unpredictable clinical course requiring immediate, often prolonged, critical care support with multiple specialists involved and frequently results in severe life-altering sequelae or death. Communication in NORSE is challenging because its etiology in a given patient is initially unknown (and often remains so), the clinical course and outcome are unpredictable, and many health care team members are involved in the care of a patient. We address the communication challenges seen in NORSE through proactive communication on 3 levels: (1) in the shared decision-making process with the family, (2) within an individual hospital, and (3) across institutions. Intentional organizational change and enhanced information dissemination may help break down barriers to effective communication. Key initiatives for enhancing information dissemination in NORSE are (1) the identification of a most responsible physician to integrate information from subspecialties, to communicate frequently and candidly with the family, and to provide continuity of care over a prolonged period of time and (2) the early involvement of palliative care services alongside ongoing therapies with curative intent to support families and the medical team in decision making and communication.  相似文献   
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