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  • 1
    Electronic Resource
    Electronic Resource
    The natural history of somatosensory and autonomic nerve dysfunction in relation to glycaemic control during the first 5 years after diagnosis of Type 1 (insulin-dependent) diabetes mellitus (1991)
    Springer
    Diabetologia 34 (1991), S. 822-829 
    Details
    ISSN: 1432-0428
    Keywords: Diabetic neuropathy ; glycaemic control ; nerve conduction ; autonomic function ; sensory thresholds
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The natural evolution of neural dysfunction was studied prospectively over 5 years following diagnosis of Type 1 (insulin-dependent) diabetes in 32 patients aged 12–36 years. Motor and sensory nerve conduction velocities, heart rate variation at rest and during deep breathing, and pupillary function were measured at diagnosis and after 3,12, 24,48, and 60 months. Thermal and vibration sensation thresholds were determined after 24, 48, and 60 months of diabetes. Mean HbA1 levels of months 3–60 within the normal range of 〈8.3% (7.3±0.2%) were observed in 13 patients (Group 1), while a mean HbA1 of months 3–60≥8.3% (10.0±0.3%) was found in 19 patients (Group 2). Mean nerve conduction was significantly diminished in Group 2 as compared with Group 1 in at least 4 out of 6 nerves tested during months 12–60 (p〈0.05). Both tests of heart rate variation were significantly impaired in Group 2 as compared with Group 1 after 24 and 60 months (p〈0.05), but no differences in pupillary function were observed between the groups. Thermal discrimination but not vibration perception thresholds on the foot were significantly higher in Group 2 than in Group 1 at 40 and 60 months (p〈0.05). Abnormalities in nerve conduction, thermal discrimination, and heart rate variation, but not vibration perception threshold and the pupillary function tests were significantly more frequent in Group 2 than in Group 1 at 60 months (p〈0.05). After 60 months, none of the patients of Group 1, but 6 and 4 patients of Group 2 developed subclinical or symptomatic neuropathy, respectively (p〈0.05). These findings suggest that the evolution of subclinical and symptomatic neuropathy during the first 5 years after diagnosis of Type 1 diabetes may be predicted by poor glycaemic control and prevented by near-normoglycaemia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00408358
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Effects of previous glycaemic control on the onset and magnitude of cognitive dysfunction during hypoglycaemia in Type 1 (insulin-dependent) diabetic patients (1992)
    Springer
    Diabetologia 35 (1992), S. 828-834 
    Details
    ISSN: 1432-0428
    Keywords: Type 1 (insulin-dependent) diabetes mellitus ; glycaemic control ; hypoglycaemia ; P300 event-relatedn potentials ; cognitive function
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary To determine whether the degree of previous glycaemic control may modify cognitive responses to hypoglycaemia, the glycaemic thresholds for, and magnitude of cognitive dysfunction as assessed by P300 event-related potentials as well as subjective and hormonal responses during hypoglycaemia were evaluated. Hypoglycaemia was induced by intravenous insulin infusion in 18 Type 1 (insulin-dependent) diabetic patients, 7 of whom were strictly controlled (HbA1c: 6.3±0.3%; mean±SEM; Group 1) and 11 of whom were poorly controlled (HbA1c: 9.1±0.4%; Group 2). Within 60 min, mean blood glucose declined from 5.6 and 5.7 mmol/l (baseline) to a nadir of 1.6 and 1.8 mmol/l followed by an increase to 5.6 and 4.3 mmol/l after 120 min in Group 1 and 2, respectively. There was no significant difference between the groups in regard to P300 latency at baseline, but between 50 and 70 min a significant prolongation of this component was noted in Group 2 as compared with Group 1 at blood glucose levels between 1.6 and 2.3 mmol/l (p〈0.05). The glycaemic thresholds at which a significant increase of P300 latency over baseline was first noted were 1.6±0.2 mmol/l in Group 1 and 3.5±0.2 mmol/l in Group 2 (p〈0.05). The glucose thresholds at which this prolongation was no longer demonstrable were 1.9±0.1 mmol/l in Group 1 and 3.8±1.4 mmol/l in Group 2, respectively (p〈0.05). The glycaemic threshold at which the P300 amplitude was first significantly reduced was 2.2 mmol/l in Group 2, whereas no such reduction was observed in Group 1. The glycaemic thresholds for the perception of subjective symptoms were 1.7±0.2 mmol/l in Group 1 and 2.5±0.2 mmol/l in Group 2 (p〈0.05), and those for the first significant rise of the counter-regulatory hormones were 2.3±0.1 and 1.6±0.2 mmol/l in Group 1 as well as 2.8±0.1 mmol/l in Group 2 (p〈0.05). Thus, the glycaemic threshold for and magnitude of, cognitive dysfunction during hypoglycaemia are reduced in strictly-controlled as compared with poorly-controlled Type 1 diabetic patients. In the latter group, cognitive impairment may precede the onset of counter-regulatory hormone responses and symptom awareness. These findings support the concept of cerebral adaptation to previous low blood glucose levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00399928
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
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