John Libbey Eurotext

The Moro reflex: insights into the pathophysiology of generalized tonic-clonic seizures and infantile spasms Article à paraître

Auteurs
1 Department of Neurology, Hospital of Merano (SABES-ASDAA), Merano-Meran, Italy
2 Department of Clinical Sciences and Community Health, Milan University, Milan, Italy
3 CRC - Center for Environmental Health, Milan University, Milan, Italy
4 Centre for Cognitive Neuroscience, European Reference Network EpiCARE, Department of Neurology, Christian Doppler University Hospital, Paracelsus Medical University of Salzburg, Salzburg, Austria
5 Neuroscience Institute, Christian Doppler University Hospital, Salzburg, Austria
6 Institute of Neuropsychological Diagnostics and Imaging, Karl Landsteiner Institute for Neurorehabilitation and Space Neurology, Salzburg, Austria
Correspondence:
Francesco Brigo
Department of Neurology, Hospital of Merano (SABESASDAA), Via Rossini, 5 – 39012 Merano-Meran, Italy.

The Moro reflex (MR) is a primitive reflex that disappears after the first three months of life. It was described by the Austrian paediatrician Ernst Moro (1874–1951) in 1918, although the earliest visual representation of the MR dates back to the first half of the 14th Century, in a fresco by Ambrogio Lorenzetti (1290-1348). The neural centre underlying the MR is located in the lower part of the brainstem since it can be elicited also in anencephalic infants, as shown by the Austrian neurologist Eduard Gamper (1887-1938) in the first medical description of anencephaly (1926). The MR is due to the activation of an archaic neural circuit present in the newborn, the activity of which is later inhibited by the upper brain structures. Given their semiological resemblance, epileptic spasms and generalized tonic-clonic seizures might be due (at least partly) to the pathological activation of the same neural archaic circuit involved in the genesis of the MR. The neuronal network underlying these different phenomena might be located in the pons. In these seizure types, the activation of the same neural circuitry involved in the MR could occur through either direct excitation or through an indirect “liberating” mechanism, secondary to epileptic disruption of cortical inhibitory control on subcortical structures. The movements of the upper extremities in epileptic spasms, in the initial phase of generalized tonic-clonic seizures, and the MR might involve a distinct neural circuitry, which is (or becomes) hyperexcitable as a consequence of a pathological condition (epilepsy) or physiological brain immaturity (the MR).