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- Baldimtsi, Evangelia, et al.
(författare)
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HbA1c and the risk of developing peripheral neuropathy in childhood-onset type 1 diabetes : A follow-up study over 3 decades
- 2024
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Ingår i: Diabetes/Metabolism Research Reviews. - : John Wiley & Sons. - 1520-7552 .- 1520-7560. ; 40:5
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Tidskriftsartikel (refereegranskat)abstract
- AIMS: We have evaluated long-term weighted mean HbA1c (wHbA1c), HbA1c variability, diabetes duration, and lipid profiles in relation to the development of diabetic peripheral neuropathy (DPN), nephropathy, and retinopathy in childhood-onset type 1 diabetes.MATERIALS AND METHODS: In a longitudinal cohort study, 49 patients (21 women) with childhood-onset type 1 diabetes were investigated with neurophysiological measurements, blood tests, and clinical examinations after a diabetes duration of 7.7 (±3.3) years (baseline) and followed with repeated examinations for 30.6 (±5.2) years. We calculated wHbA1c by integrating the area under all HbA1c values since the diabetes diagnosis. Lipid profiles were analysed in relation to the presence of DPN. Long-term fluctuations of HbA1c variability were computed as the standard deviation of all HbA1c measurements. Data regarding the presence of other diabetes complications were retrieved from medical records.RESULTS: In this follow-up study, 51% (25/49) of the patients fulfilled electrophysiological criteria for DPN. In nerve conduction studies, there was a deterioration in the amplitudes and conduction velocities for the median, peroneal, and sural nerves over time. Patients with DPN had a longer duration of diabetes, higher wHbA1c, and increased HbA1c variability. The lowest wHbA1c value associated with the development of DPN was 62 mmol/mol (7.8%). The presence of albuminuria and retinopathy was positively correlated with the presence of neuropathy.CONCLUSIONS: More than half of the patients had developed DPN after 30 years. None of the patients who developed DPN had a wHbA1c of less than 62 mmol/mol (7.8%).
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| 3. |
- Wahlgren, Carl, et al.
(författare)
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Prevalence of discomplete sensorimotor spinal cord injury as evidenced by neurophysiological methods : A cross-sectional study
- 2021
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Ingår i: Journal of Rehabilitation Medicine. - Uppsala, Sweden : Stiftelsen Rehabiliteringsinformation. - 1650-1977 .- 1651-2081. ; 53:2
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Tidskriftsartikel (refereegranskat)abstract
- OBJECTIVES: To assess the prevalence of residual trans-lesion connectivity in persons with chronic clinically complete spinal cord injury (discompleteness) by neurophysiological methods.PARTICIPANTS: A total of 23 adults with chronic sensorimotor complete spinal cord injury, identified through regional registries the regional spinal cord registry of Östergötland, Sweden.METHODS: Diagnosis of clinically complete spinal cord injury was verified by standardized neurological examination. Then, a neurophysiological examination was performed, comprising electroneurography, electromyography, sympathetic skin response and evoked potentials (sensory, laser and motor). Based on this assessment, a composite outcome measure, indicating either strong, possible or no evidence of discomplete spinal cord injury, was formed.RESULTS: Strong neurophysiological evidence of discomplete spinal cord injury was found in 17% (4/23) of participants. If also accepting "possible evidence", the discomplete group comprised 39% (9/23). The remaining 61% showed no neurophysiological evidence of discompleteness. However, if also counting reports of subjective sensation elicited during neurophysiological testing in the absence of objective findings, 52% (12/23) showed indication of discomplete spinal cord injury.CONCLUSION: Evidence of discomplete spinal cord injury can be demonstrated using standard neurophysiological techniques in a substantial subset of individuals with clinically complete spinal cord injury. This study adds to the evidence base indicating the potential of various modes of cross-lesional sensorimotor functional restoration in some cases of chronic clinically complete spinal cord injury.
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