Cortical or cortical reflex myoclonus is characterized by abnormally e
nlarged cortical somatosensory evoked potentials (giant SEPs), which m
ost likely reflect pathologically hyperexcitable sensorimotor cortex.
To clarify the pathogenesis of myoclonus of cortical origin, we simult
aneously recorded SEPs and whole head somatosensory evoked magnetic fi
elds (SEFs) following electric stimulation of the median nerve at the
wrist in six patients with cortical myoclonus. N20m and enlarged P30m
were observed in all patients and were localized at the posterior bank
of the central sulcus (Brodmann area 3b of the primary somatosensory
cortex). In addition, P25m and N35m components of SEFs were recognized
in five and four patients, respectively. P25m component, that is, the
magnetic counterpart of P25 in EEG, was the earliest cortical compone
nt showing enhancement in patients. Multidipole analysis combined with
magnetic resonance imaging (MRI) coregistration revealed that the gen
erators of P25m were in the precentral gyrus in four patients and in t
he postcentral gyrus in one patient. The second SEFs around 200 msec a
fter the single stimulus were recorded in three patients at area 3b (r
epetitive SEFs); two of whom showed negative as well as positive myocl
onus. The importance of motor cortex for the generation of cortical re
flex myoclonus was thus demonstrated. The pathologic features of SEFs
suggest abnormal excitability of primary sensorimotor cortex.