Giant early components of somatosensory evoked potentials to tibial nerve stimulation in cortical myoclonus

Abstract

Enlarged cortical components of somatosensory evoked potentials (giant SEPs) recorded by electroencephalography (EEG) and abnormal somatosensory evoked magnetic fields (SEFs) recorded by magnetoencephalography (MEG) are observed in the majority of patients with cortical myoclonus (CM). Studies on simultaneous recordings of SEPs and SEFs showed that generator mechanism of giant SEPs involves both primary sensory and motor cortices. However the generator sources of giant SEPs have not been fully understood as only one report describes clearly giant SEPs following lower limb stimulation. In our study we performed a combined EEG-MEG recording on responses elicited by electric median and tibial nerve stimulation in a patient who developed consequently to methyl bromide intoxication CM with giant SEPs to median and tibial nerve stimuli.SEPs wave shapes were identified on the basis of polarity-latency components (e.g. P15-N20-P25) as defined by earlier studies and guidelines. At EEG recording, the SEP giant component did not appear in the latency range of the first cortical component for median nerve SEP (N20), but appeared instead in the range of the P37 tibial nerve SEP, which is currently identified as the first cortical component elicited by tibial nerve stimuli. Our MEG and EEG SEPs recordings also showed that components in the latency range of P37 were preceded by other cortical components. These findings suggest that lower limb P37 does not correspond to upper limb N20. MEG results confirmed that giant SEFs are the second component from both tibial (N43m-P43m) and median (N27m-P27m) nerve stimulation. MEG dipolar sources of these giant components were located in the primary sensory and motor area.

Somatosensory-Evoked Potentials as a Marker of Functional Neuroplasticity in Athletes: A Systematic Review

“…Another limitation in deriving neurophysiological features from SEP signal amplitudes involves the fact that in group comparisons, differences in underlying tissue properties between groups potentially affect SEP amplitude. In longitudinal studies, this issue is addressed by normalizing SEP amplitudes to baseline values and then comparing changes in relative SEP amplitude between different groups (McGregor et al, 2015 ; Andrade et al, 2016 ; Anzellotti et al, 2016 ). However, in cross-sectional studies, this possibility does not exist.…”

Electrophysiological characteristics and anatomical differentiation of epileptic and non-epileptic myoclonus

“…Also, Eberhardt and Topka [17], found giant median nerve SSEP responses (P27/N35) following N20 response of normal size may be observed in some types of myoclonus. The majority of studies showed evidence of giant SSEPs only to median nerve stimulation; these giant SSEPs consisted of the increased amplitude of the components appearing after the N20, by the appearance of high amplitude complexes in the latency range of P25-N30 and P25-N30 complex [25]. These "giant" potentials can be seen in myoclonus of different origins such as PME, PHM (Lance-Adams syndrome), Alzheimer's disease, Creutzfeldt-Jakob disease, and metabolic encephalopathy [26].…”

Evoked potentials

“…Typický je nález tzv. "giant SEP" u myoklonické epilepsie, kdy hodnoty amplitud korových odpovědí SEP mohou být více než 10 uV (Anzellotti et al, 2016).…”