English
 
Help Privacy Policy Disclaimer
  Advanced SearchBrowse

Item

ITEM ACTIONSEXPORT

Released

Journal Article

Transient global ischemia specifically modulates visual P300 scalp distribution

MPS-Authors
/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;

External Resource
No external resources are shared
Fulltext (restricted access)
There are currently no full texts shared for your IP range.
Fulltext (public)
There are no public fulltexts stored in PuRe
Supplementary Material (public)
There is no public supplementary material available
Citation

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.


Cite as: https://hdl.handle.net/11858/00-001M-0000-0010-E5FB-9
Abstract
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.