Deutsch
 
Hilfe Datenschutzhinweis Impressum
  DetailsucheBrowse

Datensatz

DATENSATZ AKTIONENEXPORT

Freigegeben

Zeitschriftenartikel

Transient global ischemia specifically modulates visual P300 scalp distribution

MPG-Autoren
/persons/resource/persons20059

Ullsperger,  Markus
MPI of Cognitive Neuroscience (Leipzig, -2003), The Prior Institutes, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

/persons/resource/persons19849

Mecklinger,  Axel
MPI of Cognitive Neuroscience (Leipzig, -2003), The Prior Institutes, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

/persons/resource/persons19590

Matthes-von Cramon,  Gabi
MPI of Cognitive Neuroscience (Leipzig, -2003), The Prior Institutes, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

/persons/resource/persons20070

von Cramon,  D. Yves
MPI of Cognitive Neuroscience (Leipzig, -2003), The Prior Institutes, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

Externe Ressourcen
Es sind keine externen Ressourcen hinterlegt
Volltexte (beschränkter Zugriff)
Für Ihren IP-Bereich sind aktuell keine Volltexte freigegeben.
Volltexte (frei zugänglich)
Es sind keine frei zugänglichen Volltexte in PuRe verfügbar
Ergänzendes Material (frei zugänglich)
Es sind keine frei zugänglichen Ergänzenden Materialien verfügbar
Zitation

Ullsperger, M., Mecklinger, A., Matthes-von Cramon, G., & von Cramon, D. Y. (2000). Transient global ischemia specifically modulates visual P300 scalp distribution. Clinical Neurophysiology, 111(12), 2245-2254. doi:10.1016/S1388-2457(00)00480-6.


Zitierlink: https://hdl.handle.net/11858/00-001M-0000-0010-E5FB-9
Zusammenfassung
OBJECTIVE: Latency, amplitude, and scalp topography of the visual P300 component was examined in patients who had suffered from transient global ischemia (TGI) due to cardiac arrest and in age matched clinical and healthy controls in order to investigate the diagnostic value of this component. METHOD: Event-related potentials (ERPs) were recorded from 19 scalp electrodes in a visual oddball paradigm. RESULTS: Mean latency of the P300 component was prolonged in both patient groups. Changes in scalp distribution of the P300, however, appear to be specific to anoxic-ischemic encephalopathy. In particular, a selective reduction of the P300 amplitudes at posterior recording sites was observed in TGI patients. Moreover, examination of the auditory P300 in TGI patients revealed that this selective change seems to be restricted to the visual modality. CONCLUSION: The results are discussed with respect to selective vulnerability of brain tissue to hypoxic-ischemic injury. After TGI a modality-specific subset of P300 generators, probably located in the transitional parieto-occipital and extrastriate occipital cortex, appears to be affected. It is also noted, that the visual P300 component could serve as an additional marker of TGI especially in patients who do not show neuropathological changes in structural brain images.