Authors: Dulac O, Milh M.
Eventually, glutamate and gamma-aminobutyric acid (GABA) are both excitatory; the first cortical synapses start to appear, some myelin is found in the cerebral hemispheres, and the long tracts are barely visible. The premature activation of N-methyl-D-aspartate (NMDA) transmission seems to generate neonatal myoclonic encephalopathy. Benign neonatal seizures and migrating partial seizures of infancy may result from an excessive or premature excitability in the deep layers. Benign rolandic epilepsy and continuous spikes and waves during slow sleep are associated with an excess of excitatory and inhibitory cortical synapses. West and Lennox-Gastaut syndromes are related to an age-dependent, diffuse cortical hyperexcitability; the clinical presentation depends on the age at onset, and spike synchronization is achieved by myelination. Idiopathic generalized epilepsy is driven by brain maturation, which induces a frontal hyperexcitability responsible for myoclonic-astatic seizures at an age comprised between that of infantile and juvenile myoclonic epilepsies. The extensive physiological time frame preceding the maturation of the hippocampal-neocortical system could explain the scarcity of cortical injuries resulting from a lesion in infants.