@article{WestermaierStetterRaslanetal.2012,
  author    = {Westermaier, Thomas and Stetter, Christian and Raslan, Furat and Vinc, Giles Hamilton and Ernestus, Ralf-Ingo},
  title     = {Brain edema formation correlates with perfusion deficit during the first six hours after experimental subarachnoid hemorrhage in rats},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-75765},
  year      = {2012},
  abstract  = {Background: Severe brain edema is observed in a number of patients suffering from subarachnoid hemorrhage (SAH). Little is known about its pathogenesis and time-course in the first hours after SAH. This study was performed to investigate the development of brain edema and its correlation with brain perfusion after experimental SAH. Methods: Male Sprague-Dawley rats, randomly assigned to one of six groups (n = 8), were subjected to SAH using the endovascular filament model or underwent a sham operation. Animals were sacrificed 15, 30, 60, 180 or 360 minutes after SAH. Intracranial pressure (ICP), mean arterial blood pressure (MABP), cerebral perfusion pressure (CPP) and bilateral local cerebral blood flow (LCBF) were continuously measured. Brain water content (BWC) was determined by the wet/dry-weight method. Results: After SAH, CPP and LCBF rapidly decreased. The decline of LCBF markedly exceeded the decline of CPP and persisted until the end of the observation period. BWC continuously increased. A significant correlation was observed between the BWC and the extent of the perfusion deficit in animals sacrificed after 180 and 360 minutes. Conclusions: The significant correlation with the perfusion deficit after SAH suggests that the development of brain edema is related to the extent of ischemia and acute vasoconstriction in the first hours after SAH.},
  subject      = {Medizin},
  language  = {en}
}
@article{WiechingBenserKohlhauserVollmuthetal.2012,
  author    = {Wieching, Anna and Benser, Jasmin and Kohlhauser-Vollmuth, Christina and Weisbrich, Bendikt and Streng, Andrea and Liese, Johannes G.},
  title     = {Clinical characteristics of pediatric hospitalizations associated with 2009 pandemic influenza a (H1N1) in Northern Bavaria, Germany},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-75657},
  year      = {2012},
  abstract  = {Background: The 2009 pandemic influenza A (H1N1) (PIA) virus infected large parts of the pediatric population with a wide clinical spectrum and an initially unknown complication rate. The aims of our study were to define clinical characteristics and outcome of pandemic influenza A (H1N1) 2009-associated hospitalizations (PIAH) in children <18 years of age. All hospitalized cases of children <18 years of age with laboratory-confirmed pandemic influenza A (H1N1) 2009 in the region of Wuerzburg (Northern Bavaria, Germany) between July 2009 and March 2010 were identified. For these children a medical chart review was performed to determine their clinical characteristics and complications. Results: Between July 2009 and March 2010, 94 PIAH (62\% males) occurred in children <18 years of age, with a median age of 7 years (IQR: 3-12 years). Underlying diseases and predisposing factors were documented in 40 (43\%) children; obesity (n = 12, 30\%), asthma (n = 10, 25\%) and neurologic disorders (n = 8, 20\%) were most frequently reported. Sixteen (17\%) children received oxygen supplementation; three (3\%) children required mechanical ventilation. Six (6\%) children were admitted to an intensive care unit, four of them with underlying chronic diseases. Conclusions: Most PIAH demonstrated a benign course of disease. However, six children (6\%) needed treatment at an intensive care unit for severe complications.},
  subject      = {Medizin},
  language  = {en}
}
@article{ZellerDangWeiseetal.2012,
  author    = {Zeller, Daniel and Dang, Su-Yin and Weise, David and Rieckmann, Peter and Toyka, Klaus V. and Classen, Joseph},
  title     = {Excitability decreasing central motor plasticity is retained in multiple sclerosis patients},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-76333},
  year      = {2012},
  abstract  = {Background: Compensation of brain injury in multiple sclerosis (MS) may in part work through mechanisms involving neuronal plasticity on local and interregional scales. Mechanisms limiting excessive neuronal activity may have special significance for retention and (re-)acquisition of lost motor skills in brain injury. However, previous neurophysiological studies of plasticity in MS have investigated only excitability enhancing plasticity and results from neuroimaging are ambiguous. Thus, the aim of this study was to probe long-term depression-like central motor plasticity utilizing continuous theta-burst stimulation (cTBS), a non-invasive brain stimulation protocol. Because cTBS also may trigger behavioral effects through local interference with neuronal circuits, this approach also permitted investigating the functional role of the primary motor cortex (M1) in force control in patients with MS. Methods: We used cTBS and force recordings to examine long-term depression-like central motor plasticity and behavioral consequences of a M1 lesion in 14 patients with stable mild-to-moderate MS (median EDSS 1.5, range 0 to 3.5) and 14 age-matched healthy controls. cTBS consisted of bursts (50 Hz) of three subthreshold biphasic magnetic stimuli repeated at 5 Hz for 40 s over the hand area of the left M1. Corticospinal excitability was probed via motor-evoked potentials (MEP) in the abductor pollicis brevis muscle over M1 before and after cTBS. Force production performance was assessed in an isometric right thumb abduction task by recording the number of hits into a predefined force window. Results: cTBS reduced MEP amplitudes in the contralateral abductor pollicis brevis muscle to a comparable extent in control subjects (69 ± 22\% of baseline amplitude, p < 0.001) and in MS patients (69 ± 18\%, p < 0.001). In contrast, postcTBS force production performance was only impaired in controls (2.2 ± 2.8, p = 0.011), but not in MS patients (2.0 ± 4.4, p = 0.108). The decline in force production performance following cTBS correlated with corticomuscular latencies (CML) in MS patients, but did not correlate with MEP amplitude reduction in patients or controls. Conclusions: Long-term depression-like plasticity remains largely intact in mild-to-moderate MS. Increasing brain injury may render the neuronal networks less responsive toward lesion-induction by cTBS.},
  subject      = {Medizin},
  language  = {en}
}