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  • 1.
    Skärstrand, H
    et al.
    Lund University.
    Vaziri-Sani, Fariba
    Lunds universitet.
    Andersson, C.
    Lund University.
    Elding Larsson, H
    Lund Univeristy.
    Ivarsson, SA
    Lund University.
    Lernmark, Åke
    Lund University.
    NPY minor autoantibodies in newly diagnosed type 1 diabetes patients2013In: Diabetologia, ISSN 0012-186X, E-ISSN 1432-0428, Vol. 56, p. 19-19Article in journal (Other academic)
  • 2.
    Tallroth, G.
    et al.
    Department of Internal Medicine, University Hospital, Lund.
    Lindgren, M.
    Department of Clinical Neurophysiology, University Hospital, Lund.
    Stenberg, Georg
    Department of Clinical Neurophysiology, University Hospital, Lund.
    Rosén, Ingmar
    Department of Clinical Neurophysiology, University Hospital, Lund.
    Agardh, C. D.
    Department of Internal Medicine, University Hospital, Lund.
    Neurophysiological changes during hypoglycaemia in type 1 (insulin- dependent) diabetes mellitus and in normal man1990In: Diabetologia, ISSN 0012-186X, E-ISSN 1432-0428, Vol. 33, no 5, p. 319-323Article in journal (Refereed)
    Abstract [en]

    Hypoglycaemia (median venous blood glucose 1.8 mmol/l; range 1.6-2.3) was induced by an intravenous infusion of regular insulin in eight patients with Type 1 (insulin-dependent) diabetes mellitus (age 28.0 +/- 7.4 years; mean +/- SD, duration 15.5 +/- 5.1 years) and in 12 age- matched healthy male control subjects. Multi-channel frequency analysis of electroencephalogram (electrophysiologic brain mapping) and recording of P300 and somatosensory evoked potentials were performed before, during and immediately after the hypoglycaemic period. The hypoglycaemia produced a significant increase in low frequency electroencephalographic activity in both groups, most pronounced over anterior regions of the brain. The electroencephalographic activity was normalised immediately after the hypoglycaemic period. The patients with diabetes showed somewhat longer P300 latencies during the initial normoglycaemic examination. Hypoglycaemia caused a marked reduction of the P300 amplitude in both groups of subjects and the amplitude was not restored immediately after normalisation of blood glucose levels. The somatosensory cortical responses were not affected by hypoglycaemia. We conclude that hypoglycaemia results in impairment in cerebral function, as measured by neurophysiological techniques, which is not immediately normalised when blood glucose is restored to normal.

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