Neurophysiological changes during insulin-induced hypoglycaemia and in the recovery period following glucose infusion in type 1 (insulin-dependent) diabetes mellitus and in normal man
(1990) In Diabetologia 33(5). p.319-323- Abstract
- 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... (More)
- 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. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1105111
- author
- Tallroth, G ; Lindgren, Magnus LU ; Stenberg, Georg LU ; Rosén, Ingmar LU and Agardh, Carl-David LU
- organization
- publishing date
- 1990
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- Electroencephalogram, P300, somatosensory evoked response, hypoglycaemia, diabetes mellitus
- in
- Diabetologia
- volume
- 33
- issue
- 5
- pages
- 319 - 323
- publisher
- Springer
- external identifiers
-
- pmid:2198189
- scopus:0025342391
- ISSN
- 1432-0428
- DOI
- 10.1007/BF00403327
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Clinical Neurophysiology (013013001), Unit on Vascular Diabetic Complications (013241510), Department of Psychology (012010000)
- id
- b0f1cd22-275c-4648-9849-c508807db37d (old id 1105111)
- date added to LUP
- 2016-04-01 12:10:39
- date last changed
- 2021-09-26 04:55:41
@article{b0f1cd22-275c-4648-9849-c508807db37d,
abstract = {{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.}},
author = {{Tallroth, G and Lindgren, Magnus and Stenberg, Georg and Rosén, Ingmar and Agardh, Carl-David}},
issn = {{1432-0428}},
keywords = {{Electroencephalogram; P300; somatosensory evoked response; hypoglycaemia; diabetes mellitus}},
language = {{eng}},
number = {{5}},
pages = {{319--323}},
publisher = {{Springer}},
series = {{Diabetologia}},
title = {{Neurophysiological changes during insulin-induced hypoglycaemia and in the recovery period following glucose infusion in type 1 (insulin-dependent) diabetes mellitus and in normal man}},
url = {{http://dx.doi.org/10.1007/BF00403327}},
doi = {{10.1007/BF00403327}},
volume = {{33}},
year = {{1990}},
}