The 'excitability' and 'conductivity' of motor pathways during transcranial stimulation (TCS) have been investigated in 49 patients affected by multiple sclerosis (34), amyotrophic lateral sclerosis ...(7), spino-cerebellar ataxia (3), primary lateral sclerosis (4) and brain metastasis (1). Hyper-reflexia, spasticity and weakness were correlated with the central motor conduction time (CCT) and with the threshold intensity of TCS required to produce a motor evoked potential (MEP). MEPs to magnetic TCS were recorded from hand and foot muscles during relaxation, contraction and after tendon vibration. Thresholds and CCTs of the patients were compared with those of 30 healthy controls. Increased threshold was found in 37 out of 49 patients (75.5%). Prolongation of the CCT was found in 38 out of 63 clinically affected upper limbs (60.3%) and in 56 out of 77 clinically affected lower limbs (72.7%). Absent motor responses to maximal TCS were found in 20 out of 98 lower limbs (20.4%). Excluding ALS patients (in whom there was a lower threshold for MEP elicitation), a significant linear correlation was found between prolonged CCT and increased threshold. While MEPs with prolonged CCTs have elevated TCS threshold, it is important to note that an elevated threshold was found in 14 out of 49 patients (28.5%) despite unchanged CCT. Spasticity and/or hyper-reflexia were more frequently associated with increased threshold than with prolonged CCT, while weakness was correlated equally well with both these parameters. In this respect magnetic TCS proves to represent a new tool for the detection of abnormal 'excitability' of the central motor tracts.
Motor evoked potentials (MEPs) to transcranial stimulation (TCS) and somatosensory evoked potentials to median nerve stimulation (MN-SEPs) were examined in 74 patients affected by multiple sclerosis ...(MS = 49 cases), amyotrophic lateral sclerosis (ALS = 9 cases), cervical cord lesions (7 cases), Parkinson's disease (PD = 5 cases), Huntington's chorea (HC = 2 cases), Wilson's disease (WD = 1 case), subacute combined degeneration (SCD = 1 case). MN-SEPs were altered in 38% of arms in MS with a higher incidence in clinically affected than in clinically 'silent' arms (= 77.8% vs. 27.5%). MEP alterations were found in 54% of examined arms, mostly because of a prolongation of the motor CCT. This index was invariably altered in the affected arms, whilst it was involved in 40% of the 'silent' ones. Twelve out of 18 arms displayed abnormal MEPs in ALS. These were mainly due to an absent response, even if moderate motor CCT prolongation and 'giant' MEPs were also encountered. MN-SEPs were altered in 3/18 arms. By recording MEPs from proximal and distal upper limb muscles, cues on the level of abnormal propagation were obtained in patients suffering from 'focal' lesions of the spinal cord. Combining SEP records enhanced the diagnostic yield in this field. Both MEPs and SEPs were normal in patients with PD and HC, whilst abnormally prolonged CCTs were found in the case with WD. MEP and SEP recording revealed central propagation abnormalities coupled to a severe clinical picture of the peripheral nerve involvement (as in the case of SCD).
