Objective Dietary proteins raise blood glucose levels; dietary fats delay this rise. We sought to assess the insulin amount required to normalize glucose levels after a fat- and protein-rich meal (FPRM). Methods Sixteen adolescents (5 female) with type 1 diabetes (median age: 18.2 years; range: 15.2–24.0; duration: 7.1 years; 2.3–14.3; HbA1c: 7.2%; 6.2–8.3%) were included. FPRM (carbohydrates 57 g; protein 92 g; fat 39 g; fibers 7 g; calories 975 Kcal) was served in the evening, with 20 or 40% extra insulin compared to a standard meal (SM) (carbohydrates 70 g; protein 28 g; fat 19 g; fibers 10 g; calories 579 Kcal) or carbohydrates only. Insulin was administered for patients on intensified insulin therapy or as a 4-hour-delayed bolus for those on pump therapy. The 12-hour post-meal glucose levels were compared between FPRM and SM, with the extra insulin amount calculated based on 100 g proteins as a multiple of the carbohydrate unit. Results Glucose levels (median, mg/dL) 12-hour post-meal with 20% extra insulin vs. 40% vs. insulin dose for SM were 116 vs. 113 vs. 91. Glucose-AUC over 12-hour post-meal with 20% extra insulin vs. 40% vs. insulin dose for SM was 1603 mg/dL/12 h vs. 1527 vs. 1400 (no significance). Glucose levels in the target range with 20% extra insulin vs. 40% were 60% vs. 69% (p=0.1). Glucose levels <60 mg/dL did not increase with 40% extra insulin. This corresponds to the 2.15-fold carbohydrate unit for 100 g protein. Conclusions We recommend administering the same insulin dose given for 1 carbohydrate unit (10 g carbs) to cover 50 g protein.

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Aims. Attention deficit hyperactivity disorder (ADHD) is one of the most frequent neurocognitive impairments in neurofibromatosis type 1 (NF1) and a well-known risk factor for intellectual dysfunction in general. Since NF1 is per se associated with intellectual difficulties, this comorbidity may be crucial for the cognitive development of affected patients. In our study, we investigated if attention deficits are associated with intellectual functioning in NF1 and if children with NF1 plus ADHD differ in their intellectual and attention profiles from children affected by NF1-only or ADHD only. Methods. 111 children aged between 6 and 12 years (53 NF1 plus ADHD, 28 NF1-only, 30 ADHD-only) performed the German version of the intelligence test WISC-IV and a continuous performance test (T.O.V.A.) to assess attention functions. Parents completed questionnaires about everyday attention and executive functions (Conners 3®, BRIEF). Results. Children with NF1 plus ADHD showed significantly lower intelligence test scores (full-scale IQ: 89.39 [1.40]) than patients with NF1-only (full-scale IQ: 101.14 [1.98]; p<.001), and intellectual functioning correlated significantly with attention performance in NF1 (p<.001). As compared to NF1-only, attention, and executive functioning were impaired on several dimensions (T.O.V.A., Conners 3® and BRIEF) in NF1 plus ADHD. ADHD-only was associated with significantly higher problem scores regarding hyperactivity/impulsivity and inattention (Conners 3®). NF1-only was associated with inattentiveness when compared to the normative sample of the T.O.V.A. Conclusion. NF1 is associated with variable attention problems. Severe attention deficits appear to be a risk factor for intellectual dysfunction in NF1, more than NF1 without attention deficit. NF1 plus ADHD presents a specific cognitive profile, which differs from that of NF1 and from neurotypical ADHD.

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Background: The risk factors for impaired cognitive development after unilateral perinatal stroke are poorly understood. Non-verbal intelligence seems to be at particular risk, since language can shift to the right hemisphere and may thereby reduce the capacity of the right hemisphere for its originary functions. Pharmaco-refractory epilepsies, a frequent complication of perinatal strokes, often lead to impaired intelligence. Yet, the role of well-controlled epilepsies is less well-understood. Here, we investigated whether well-controlled epilepsies, motor impairment, lesion size, lesion side, and lateralization of language functions influence non-verbal functions.Methods: We recruited 8 patients with well-controlled epilepsies (9–26 years), 15 patients without epilepsies (8–23 years), and 23 healthy controls (8–27 years). All underwent the Test of Non-verbal Intelligence, a motor-independent test, which excludes biased results due to motor impairment. Language lateralization was determined with functional MRI, lesion size with MRI-based volumetry, and hand motor impairment with the Jebson-Taylor Hand Function-Test.Results: Patients with epilepsies showed significantly impaired non-verbal intelligence [Md = 89.5, interquartile range (IQR) = 13.5] compared with controls (Md = 103, IQR = 17). In contrast, patients without epilepsies (Md = 97, IQR = 15.0) performed within the range of typically developing children. A multiple regression analysis revealed only epilepsy as a significant risk factor for impaired non-verbal functions.Conclusion: In patients with unilateral perinatal strokes without epilepsies, the neuroplastic potential of one healthy hemisphere is able to support the development of normal non-verbal cognitive abilities, regardless of lesion size, lesion side, or language lateralization. In contrast, epilepsy substantially reduces this neuroplastic potential; even seizure-free patients exhibit below-average non-verbal cognitive functions.