TY - JOUR
T1 - Cortical excitability changes associated with fixation-off sensitivity
T2 - A case report
AU - Strigaro, Gionata
AU - Prandi, Paolo
AU - Varrasi, Claudia
AU - Monaco, Francesco
AU - Cantello, Roberto
PY - 2011/8
Y1 - 2011/8
N2 - "Fixation-off sensitivity" (FOS) is an ideal human model for studying the features of epileptic discharges. Physiologically, FOS is expected to correspond to enhanced excitability of widespread cortical structures. To test this hypothesis, we measured by transcranial magnetic stimulation (TMS), the excitability level of the primary motor area in a 22-year-old woman with eyelid myoclonias and absences, who presented with generalized FOS. We also explored her visual system by pattern-reversal and flash-visual evoked potentials (VEPs). Both outside and within FOS, the cortical silent period was dramatically short, indicating defective γ-aminobutyric acid (GABA) B inhibition as a persistent background factor. The same was true for the short-interval intracortical inhibition, a TMS marker of cortical GABA A inhibition. The FOS state corresponded then to a pathologic enhancement of intracortical facilitation, a TMS marker of Glu/Asp transmission. During FOS, the flash VEP exhibited a hugely enhanced afterdischarge, expressing a pathologic overactivity of secondary visual areas. Within the limits of a single-case study, we thus provide electrophysiologic evidence supporting a grossly imbalanced cortical excitability, in both the frontal and posterior areas, as an important correlate of the present FOS subtype.
AB - "Fixation-off sensitivity" (FOS) is an ideal human model for studying the features of epileptic discharges. Physiologically, FOS is expected to correspond to enhanced excitability of widespread cortical structures. To test this hypothesis, we measured by transcranial magnetic stimulation (TMS), the excitability level of the primary motor area in a 22-year-old woman with eyelid myoclonias and absences, who presented with generalized FOS. We also explored her visual system by pattern-reversal and flash-visual evoked potentials (VEPs). Both outside and within FOS, the cortical silent period was dramatically short, indicating defective γ-aminobutyric acid (GABA) B inhibition as a persistent background factor. The same was true for the short-interval intracortical inhibition, a TMS marker of cortical GABA A inhibition. The FOS state corresponded then to a pathologic enhancement of intracortical facilitation, a TMS marker of Glu/Asp transmission. During FOS, the flash VEP exhibited a hugely enhanced afterdischarge, expressing a pathologic overactivity of secondary visual areas. Within the limits of a single-case study, we thus provide electrophysiologic evidence supporting a grossly imbalanced cortical excitability, in both the frontal and posterior areas, as an important correlate of the present FOS subtype.
KW - Cortical excitability
KW - Fixation-off sensitivity
KW - Transcranial magnetic stimulation
KW - Visual evoked potentials
UR - http://www.scopus.com/inward/record.url?scp=79960909790&partnerID=8YFLogxK
U2 - 10.1111/j.1528-1167.2011.03122.x
DO - 10.1111/j.1528-1167.2011.03122.x
M3 - Article
SN - 0013-9580
VL - 52
SP - e89-e92
JO - Epilepsia
JF - Epilepsia
IS - 8
ER -