|
Findings |
Affected region |
Mechanisms |
References |
|
Fetus from GDM |
| Anencephaly, holoprosencephaly, syntelencephaly |
CNS |
Increased oxidative stress |
[147] |
| Neural tube defects |
CNS |
Hyperinsulinemia-increasedoxidative stress |
[148] |
| CNS malformations |
CNS |
Hyperglycaemia |
[149] |
|
Infants from GDM |
| Increasedlatency invisual evoked potentials |
Visual cortex |
nr |
[102] |
| Alterations inthe pattern ofevent-related potentials |
CNS |
nr |
[103] |
| Impairedrecognition memory |
Hippocampus |
Alterations inevent-related potentials |
[106] |
| Motor deficit, inattention |
CNS |
nr |
[100] |
| Impairedrecognition memory |
CNS |
Iron deficiency |
[15] |
| Impairedrecognition memory |
Hippocampus |
Changesofevent-related potentials |
[16] |
| No differencein the potentials ofauditory response |
Brainstem |
nr |
[150] |
| Alterations inevent-related memory |
CNS |
Deficitin rememberingsequencesofevents with multiplesteps |
[151] |
| Motor deficit, inattention |
CNS |
Correlates with the mother glycaemic control |
[101] |
| Poor performancein neurologicaltests |
CNS |
Not correlated withmaternalglycaemic control |
[100] |
| Motor deficit |
CNS |
Correlated with the maternal glycaemic control |
[152] |
