The Glasgow Coma Scale: time for critical reappraisal?

نویسندگان

  • Steven Laureys
  • Olivier Bodart
  • Olivia Gosseries
چکیده

www.thelancet.com/neurology Vol 13 August 2014 755 in astrocytes. Furthermore, KIR4.1 loss will also occur when oligodendrocytes are lost in the demyelinating process or astrocyte processes are damaged by mechanisms independent of antibody-mediated and complement-mediated immune reactions. Finally, technical issues of immunocytochemistry (eg, use of frozen vs paraffi n sections) and exact staging of lesions might partly diff er between the studies. Do these fi ndings, from independent research groups, mean that research into KIR4.1 in multiple sclerosis should end? We hope not. The reasons for the discrepancies between the investigations might be at least partly technical and call for additional work. Pathological studies using diff erent analytical approaches are also warranted to deepen the understanding of this potentially revolutionary aspect of multiple sclerosis research. Many unanswered questions related to KIR4.1 function still remain. The coexpression of KIR4.1 and aquaporin-4 channels in endfeet of astrocytes and their synergistic eff ect in maintaining osmotic homoeostasis is intriguing, especially when considering that most retinal pathological changes characterised by Müller cell damage are accompanied by changes of the amount or spatial distribution of both channels. Finally, the potential relation between anti-KIR4.1 antibodies and a more general dysfunction of immune-mediated mechanisms in patients with multiple sclerosis deserves further investigation.

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عنوان ژورنال:
  • The Lancet. Neurology

دوره 13 8  شماره 

صفحات  -

تاریخ انتشار 2014