17 research outputs found

    Case report: Psychosis and catatonia in an adolescent patient with adipsic hypernatremia and autoantibodies against the subfornical organ.

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    This is the first description of a patient in which adipsic hypernatremia, a rare autoimmune encephalitis, presented in combination with complex psychiatric symptomatology, including psychosis and catatonia. Adipsic hypernatremia is characterized by autoantibodies against the thirst center of the brain. These autoantibodies cause inflammation and apoptosis in key regions of water homeostasis, leading to lack of thirst and highly increased serum sodium. To date, the symptoms of weakness, fatigue and drowsiness have been associated with adipsic hypernatremia, but no psychiatric symptomatology. Here, we showcase the first description of an adolescent patient, in which severe and complex psychiatric symptoms presented along with adipsic hypernatremia. The patient experienced delusion, hallucinations, restlessness and pronounced depression. Further, he showed ritualized, aggressive, disinhibited and sexualized behavior, as well as self-harm and psychomotor symptoms. Due to his severe condition, he was hospitalized on the emergency unit of the child and adolescent psychiatry for 8 months. Key symptoms of the presented clinical picture are: childhood-onset complex and treatment-resistant psychosis/catatonia, pronounced behavioral problems, fatigue, absent thirst perception, hypernatremia and elevated prolactin levels. This case report renders first evidence speaking for a causal link between the autoimmune adipsic hypernatremia and the psychotic disorder. Moreover, it sheds light on a new form of autoimmune psychosis

    ISLES 2015 - A public evaluation benchmark for ischemic stroke lesion segmentation from multispectral MRI

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    Ischemic stroke is the most common cerebrovascular disease, and its diagnosis, treatment, and study relies on non-invasive imaging. Algorithms for stroke lesion segmentation from magnetic resonance imaging (MRI) volumes are intensely researched, but the reported results are largely incomparable due to different datasets and evaluation schemes. We approached this urgent problem of comparability with the Ischemic Stroke Lesion Segmentation (ISLES) challenge organized in conjunction with the MICCAI 2015 conference. In this paper we propose a common evaluation framework, describe the publicly available datasets, and present the results of the two sub-challenges: Sub-Acute Stroke Lesion Segmentation (SISS) and Stroke Perfusion Estimation (SPES). A total of 16 research groups participated with a wide range of state-of-the-art automatic segmentation algorithms. A thorough analysis of the obtained data enables a critical evaluation of the current state-of-the-art, recommendations for further developments, and the identification of remaining challenges. The segmentation of acute perfusion lesions addressed in SPES was found to be feasible. However, algorithms applied to sub-acute lesion segmentation in SISS still lack accuracy. Overall, no algorithmic characteristic of any method was found to perform superior to the others. Instead, the characteristics of stroke lesion appearances, their evolution, and the observed challenges should be studied in detail. The annotated ISLES image datasets continue to be publicly available through an online evaluation system to serve as an ongoing benchmarking resource (www.isles-challenge.org).Peer reviewe

    Ready for change: Oscillatory mechanisms of proactive motor control

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    <div><p>Proactive motor control is a preparatory mechanism facilitating upcoming action inhibition or adaptation. Previous studies investigating proactive motor control mostly focused on response inhibition, as in the classical go-nogo or stop-signal tasks. However, everyday life rarely calls for the complete suppression of actions without subsequent behavioral adjustment. Therefore, we conducted a modified cued go-nogo-change task, in which cues indicated whether participants might have to change to an alternative action or inhibit the response to an upcoming target. Based on the dual-mechanisms of control framework and using electroencephalography (EEG), we investigated the role of the sensorimotor cortex and of prefrontal regions in preparing to change and cancel motor responses. We focused on mu and beta power over sensorimotor cortex ipsi- and contralateral to an automatic motor response and on prefrontal beta power. Over ipsilateral sensorimotor cortex, mu and beta power was relatively decreased when anticipating to change or inhibit the automatic motor behavior. Moreover, alpha phase coupling between ipsilateral motor cortex and prefrontal areas decreased when preparing to change, suggesting a decoupling of sensorimotor regions from prefrontal control. When the standard motor action actually had to be changed, prefrontal beta power increased, reflecting enhanced cognitive control. Our data highlight the role of the ipsilateral motor cortex in preparing to inhibit and change upcoming motor actions. Here, especially mu power and phase coupling seem to be critical to guide upcoming behavior.</p></div

    Target-evoked prefrontal beta power (15–25 Hz).

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    <p>(A) Timecourse of beta power at left and right prefrontal clusters. As shaded area the SEM is displayed and the time-window we analyzed (200–500 ms) is marked with a grey box. Significant differences are indicated with asterisks. (B) At both left and right prefrontal clusters beta power was higher in change- and nogo- than no-change-/no-nogo-trials and lowest in go-trials. As error bars the SEM is depicted. (C) Topographic plots show the scalp distribution of the mean signal change (200–500 ms) in the beta band as difference between conditions.</p

    Design and behavioral results.

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    <p>(A) Design of the cued go-nogo-change task. In expecting go-trials, the cue (black square) was always followed by a black triangle, indicating a right button press. In expecting change-trials, the cue (green square) was followed in 75% by a black triangle, indicating a right button press and in 25% by a green triangle, indicating a left button press. In expecting nogo-trials, the cue (red square) was followed in 75% by a black triangle, indicating a right button press and in 25% by a red triangle, indicating no button press. In the second half of the experiment, the matching of the response buttons was reversed (meaning expecting go-trials required a left button press etc.). (B) Reaction times. Mean reaction times in ms in go-, no-change-, no-nogo- and change-trials. As error bars the standard error of the mean (SEM) is depicted. Participants responded faster in go- than no-change-/no-nogo- than change-trials. Significant effects are indicated with asterisks (* for ≀ 0.05, ** for ≀ 0.01, *** for ≀ 0.001).</p

    Alpha coupling effects.

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    <p>(A) Alpha coupling between 900–1100 ms is shown. Displayed connections show significantly increased coupling from ipsilateral motor cortex to corresponding electrodes for EG- compared to EC-trials and for EN- compared to EC-trials. (B) Exemplary time-courses of the PLV. On the left, synchrony between contralateral motor cortex and a same-side prefrontal electrode (F5/F6) and on the right synchrony between ipsilateral motor cortex and a same-side prefrontal electrode (F5/F6) is displayed. Note that there was a significant difference for connectivity to ipsilateral but not to contralateral M1.</p

    Sensorimotor effects in the cue-target interval.

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    <p>(A) On the left timecourses of mu (9-14 Hz) and beta (15–25 Hz) power at contralateral and ipsilateral sensorimotor clusters in relation to the standard motor response are displayed. The modulation of mu power was strongest over the ipsilateral hemisphere. Between 500–1100 ms mu increased in expecting go (EG), was around baseline in expecting nogo (EN) and decreased clearly in expecting change (EC). As shaded area around the mean, the SEM is displayed. Target onset was at 1100 ms (dotted line). Horizontal bars under the time axis highlight time-windows with significant differences between conditions. Black bars highlight windows where EG & EC significantly differed, dark grey bars where EG & EN differed and light grey bars where EN & EC differed. To the right bar graphs show mean mu/beta power between 500–1100 ms at contralateral and ipsilateral sensorimotor sites. As error bars the SEM is depicted. Significant differences are stressed with asterisks. (B) Time-frequency plots of activity in the EG condition at contra- and ipsilateral sensorimotor clusters. (C) The topographic plots show the scalp distribution of the mean signal change (500–1100 ms) as differences between EC and EG. All data in this figure is flipped along the midline.</p
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