@article {2131, title = {Transition from the locked in to the completely locked-in state: a physiological analysis.}, journal = {Clin Neurophysiol}, volume = {122}, year = {2011}, month = {06/2011}, pages = {925-33}, abstract = {

OBJECTIVE:\ 

To clarify the physiological and behavioral boundaries between locked-in (LIS) and the completely locked-in state (CLIS) (no voluntary eye movements, no communication possible) through electrophysiological data and to secure\ brain-computer-interface\ (BCI) communication.

METHODS:\ 

Electromyography from facial muscles, external anal sphincter (EAS), electrooculography and electrocorticographic data during different psychophysiological tests were acquired to define electrophysiological differences in an amyotrophic lateral sclerosis (ALS) patient with an intracranially implanted grid of 112 electrodes for nine months while the patient passed from the LIS to the CLIS.

RESULTS:\ 

At the very end of the LIS there was no facial muscle activity, nor external anal sphincter but eye control. Eye movements were slow and lasted for short periods only. During CLIS event related\ brainpotentials (ERP) to passive limb movements and auditory stimuli were recorded, vibrotactile stimulation of different body parts resulted in no ERP response.

CONCLUSIONS:\ 

The results presented contradict the commonly accepted assumption that the EAS is the last remaining muscle under voluntary control and demonstrate complete loss of eye movements in CLIS. The eye muscle was shown to be the last muscle group under voluntary control. The findings suggest ALS as a multisystem disorder, even affecting afferent sensory pathways.

SIGNIFICANCE:\ 

Auditory and proprioceptive\ brain-computer-interface\ (BCI) systems are the only remaining communication channels in CLIS.

}, keywords = {Adult, Amyotrophic Lateral Sclerosis, Area Under Curve, Brain, Communication Aids for Disabled, Disease Progression, Electroencephalography, Electromyography, Humans, Male, Signal Processing, Computer-Assisted, User-Computer Interface}, issn = {1872-8952}, doi = {10.1016/j.clinph.2010.08.019}, url = {http://www.ncbi.nlm.nih.gov/pubmed/20888292}, author = {Murguialday, A Ramos and Jeremy Jeremy Hill and Bensch, M and Martens, S M M and S Halder and Nijboer, F and Schoelkopf, Bernhard and Niels Birbaumer and Gharabaghi, A} } @article {3414, title = {Pathways for the regulation of body iron homeostasis in response to experimental iron overload.}, journal = {J Hepatol}, volume = {43}, year = {2005}, month = {10/2005}, pages = {711-9}, abstract = {BACKGROUND/AIMS: Secondary iron overload is a frequent clinical condition found in association with multiple blood transfusions. METHODS: To gain insight into adaptive changes in the expression of iron genes in duodenum, liver and spleen upon experimental iron overload we studied C57BL/6 mice receiving repetitive daily injections of iron-dextran for up to 5 days. RESULTS: Iron initially accumulated in spleen macrophages but with subsequent increase in macrophage ferroportin and ferritin expression its content in the spleen decreased while a progressive storage of iron occurred within hepatocytes which was paralleled by a significant increase in hepcidin and hemojuvelin expression. Under these conditions, iron was still absorbed from the duodenal lumen as divalent metal transporter-1 expressions were high, however, most of the absorbed iron was incorporated into duodenal ferritin, while ferroportin expression drastically decreased and iron transfer to the circulation was reduced. CONCLUSIONS: Experimental iron overload results in iron accumulation in macrophages and later in hepatocytes. In parallel, the transfer of iron from the gut to the circulation is diminished which may be referred to interference of hepcidin with ferroportin mediated iron export, thus preventing body iron accumulation.}, keywords = {Animals, Disease Models, Animal, Disease Progression, DNA Primers, Duodenum, Gene Expression Regulation, Hepatocytes, Homeostasis, Iron, Iron Overload, Macrophages, Mice, Mice, Inbred C57BL, Polymerase Chain Reaction, RNA}, issn = {0168-8278}, doi = {10.1016/j.jhep.2005.03.030}, url = {http://www.sciencedirect.com/science/article/pii/S0168827805003168$\#$}, author = {Theurl, Igor and Ludwiczek, Susanne and Eller, Philipp and Seifert, Markus and Artner, Erika and Peter Brunner and Weiss, G{\"u}nter} }