ABNORMALITIES OF THE BALANCE BETWEEN INHIBITION AND EXCITATION IN THE, MOTOR CORTEX OF PATIENTS WITH CORTICAL MYOCLONUS

Patients with cortical myoclonus may have purely focal or multifocal j erks, or they may have additional bilateral or generalized jerks, sugg esting the spread of excitatory myoclonic activity between the cerebra l hemispheres and across the sensorimotor cortex. The factors contribu ting to this spread of activity were investigated in 10 patients with multifocal cortical myoclonus and eight patients with multifocal and b ilateral or generalized cortical myoclonus. The two groups were termed 'non-spreaders' and 'spreaders', respectively. Eight of the patients were also epileptic. Motor thresholds to single transcranial magnetic shocks at rest were higher in 'non-spreaders' (median 88%, range 45-10 0% of stimulator output) than either 'spreaders' (50%, range 26-90%, P = 0.0231 or healthy controls (38%, range 28-53%, P < 0.001). This pat hological elevation in motor threshold was not simply an effect of tre atment with antiepileptic drugs. Paired transcranial magnetic stimuli were used to investigate ipsilateral cortico-cortical and transcallosa l inhibition. There was less (MANOVA, P < 0.05) ipsilateral inhibition at interstimulus intervals (ISIs) of 1-6 ms in 'spreaders' (mean 107/-SEM 23% of control) compared with 'non-spreaders' (75+/-15%) or heal thy subjects (59+/-10%1. There was also less (P < 0.05) transcallosal inhibition across inhibitory timings (10, 12 and 14 ms) in the 'spread ers' (98+/-6% of control) compared with the 'non-spreaders' (64+/-8%) or healthy subjects (59+/-6%). There was no relationship between ipsil ateral cortico-cortical and transcallosal inhibition and the presence or absence of epilepsy, although non-epileptic patients did have highe r motor thresholds (median 85%, range 32-100% of stimulator output) th an either epileptic patients (50%, range 26-90%, P < 0.001) or healthy controls (38%, range 28-53%, P = 0.002). Abnormalities in ipsilateral and transcallosal inhibition appear to facilitate the spread of the c ortical myoclonic activity responsible for bilateral and generalized j erks. However these abnormalities in inhibition do not play a major ro le in the development of generalized seizures in patients with cortica l myoclonus.