Scalp topography of somatosensory evoked potentials following electrical stimulation of femoral nerve

Up to 29 channels of somatosensory evoked potentials (SEPs) were recorded in 10 normal volunteers following unilateral femoral nerve (FN) and tibial nerve (TN) electrical stimulation. Typical short latency FN SEPs consisted of 6 components, P15, N19, P26, N34, P44 and N56. P15 and N19 were widely distributed on the scalp. The first localized scalp component, P26, was strictly postrolandic and distributed on the contralateral parietal scalp close to midline with a prerolandic phase reversal, N26. This scalp distribution is clearly different from the first localized potential of tibial nerve SEPs. N34 and P44 were maximal at the vertex with a distribution that spread to the ipsilateral central and parietal scalp. The amplitude of P26 increased and latency shortened with increasing stimulus intensity and both values plateaued after the stimulus intensity reached motor threshold. No correlation was found between the peak latency of P26 and body height.     

Scalp topography and distribution of cortical somatosensory evoked potentials to median nerve stimulation

Topographies and distributions of cortical SEPs to median nerve stimulation were studied in 8 normal adults and 5 neurological patients. SEPs recorded from C4, P4, Pz, T6-A1A2 derivations to left median nerve stimulation were composed of 2 early negative (N16, N20) and 2 positive components (P12, P23), whereas those recorded from frontal electrodes (Fz, Fp1, Fp2) disclosed 2 early negativities (N16, N24) and 2 early positivities (P12, P20). N20 and P20, and P23 and N24, reversed across the rolandic fissure with no significant difference in their peak latencies. P23 was of slightly shorter latency at C4 than at more posterior electrodes (P4, T6, Pz). In 3 patients with complete hemiplegia but normal sensation, all the early SEP components were normal in scalp distribution and peak latencies except for a decrease of N24 amplitude. In 2 patients with complete hemiplegia and sensory loss no early cortical SEPs were seen. These findings suggest that N20 and P20 are generated as a single horizontal dipole in the central fissure, whereas P23 and N24 are a reflection of multiple generators in pre- and postrolandic regions.     

The effect of pentobarbital on central somatosensory conduction time in the rat

Somatosensory evoked potentials (SEPs) were recorded from skull electrodes in the rat. Central somatosensory conduction time was estimated by subtracting the peak latency of component II which is generated from the dorsal column nuclei and medial lemniscus from that of the primary cortical response. The mean was 2.67 +/- 0.10 msec during light pentobarbital anaesthesia. SEPs recorded during moderate anaesthesia showed delays of nearly 1 msec in anterior component III from the thalamus and sensory radiation, and the subsequent cortical potentials.     

Central and peripheral conduction times in multiple sclerosis

Somatosensory evoked potentials (SEPs) were recorded simultaneously from the cervical spine and scalp in 25 normal subjects and 105 patients with established or suspected multiple sclerosis (MS) using median nerve stimulation. The normal latency of the main peak of the cervical SEP (N14) following median nerve stimulation at the wrist was 13.7 +/- 0.8 msec. The peak latency of the first cortical event of the scalp SEP (N20) was 19.1 +/- 0.9 msec. The difference in these latencies (N20 -- N14) reflects a conduction time between the dorsal column nuclei and cortex. It measured 5.45 +/- 0.7 msec. The conduction times between the wrist and Erb's point and Erb's point and N14 measured 8.6 +/- 0.7 msec and 5.1 +/- 0.6 msec respectively. There was a 68.6% overall incidence of abnormalities of N14, N20 or (N20 -- N14) in the patients. This incidence was over 80% in definite and early probable or latent MS, 68.2% in progressive spinal MS and 40.0% in suspects. SEPs were also simultaneously recorded from the lower thoracic spine (T12) and scalp in a different group of 25 normal subjects using tibial nerve stimulation. The latency of the thoracic SEP (N21) was 21.4 +/- 1.5 msec and that of the first cortical event of the scalp SEP (P40) was 38.6 +/- 2.2 msec. The difference in these latencies (P40 -- N21) which reflects conduction between T12 and the cortex measured 17.2 +/- 1.7 msec. Conduction between the ankle and popliteal fossa was 7.0 +/- 0.65 msec and between the popliteal fossa and N21, it was 14.5 +/- 1.1 msec. All of a small group of MS suspects showed abnormality of P40 or (P40 -- N21).     

Somatosensory evoked potentials in the term newborn.

Median nerve somatosensory evoked potentials (SEPs) were recorded from surface electrodes in 40 healthy term infants (range 36.5-43 weeks postmenstrual age). Electrical stimulation at 5 Hz was used, averaging the response to several runs of 1024 stimuli to each median nerve, bandpass 10-3000 Hz, sweeptime 100 msec. Identifiable potentials were collected over the cervical cord on all runs in all 40 infants and from the cortex in at least some runs in 39 out of 40 infants. The cervical response showed little variation and consisted of a clear negative wave with up to 3 peaks, mean latency of the largest 10.2 +/- 0.7 msec, followed by a positive deflection. The cortical response was very variable in form and latency between infants and to a lesser degree within infants. Four types of cortical wave form were found, symmetrical, asymmetrical, plateau and M shaped, of increasing complexity. In 11% of trials the response was absent or indistinct but could usually be uncovered by alteration in stimulus frequency or intensity. In the whole group, the mean latency for N1 was 30.0 +/- 6.8 msec and for the central conduction time 19.8 +/- 6.5 msec. Significant differences were found between the 4 cortical wave forms in the main variables measured, which gave support for form S being the most primitive and form M the most mature response.     

Motor and somatosensory evoked potentials in Autosomal Dominant Hereditary Spastic Paraparesis (ADHSP) linked to chromosome 2p, SPG4

The aim of our study was to evaluate Motor Evoked Potentials (MEPs) and cortical excitability, using Transcranial Magnetic Stimulation (TMS) as well as short latency Somatosensory Evoked Potentials (SEPs) in Autosomal Dominant Hereditary Spastic Paraparesis (ADHSP) patients. MEPs were recorded from upper and lower limb muscles in 12 patients (7 m and 5f) affected by ADHSP with spastin mutation (SPG4). We measured: (i) motor threshold (MTh); (ii) total motor conduction time (TMCT); (iii) direct and indirect central motor conduction time (d-CMCT and i-CMCT) calculated by subtracting from the cortical latency those obtained on magnetic spinal stimulation (d-PMCT) and via the F-wave method (i-PMCT); (iv) MEP amplitude (MEP/Mmax ratio%) and (v) duration of the cortical silent period (CSP). Latency, amplitude and persistence of the F-wave obtained with electrical nerve stimulation were also considered; H reflex was also tested from lower extremities. SEPs were recorded from spine and scalp sites following median and posterior tibial nerve stimulation; conventional latency and amplitude measurements were performed. In a comparison with the control group, the MTh recording from lower limbs was significantly higher (67.5 +/- 7.7% versus 52.5 +/- 6.9%), MEPs were absent in one case and showed reduced amplitude in the remainders (22.9 +/- 12.6% versus 66.3 +/- 25.9% of M wave); TMCT resulted to be abnormal (36.5 +/- 3.9 ms versus 27.1 +/- 1.4 ms) and d-CMCT as well as i-CMCT were significantly prolonged (23.1 +/- 3.5 ms versus 13.8 +/- 1.3 ms; and 20.1 +/- 3.4 ms versus 10.6 +/- 1.3 ms, respectively). The CSP, which was normal from the hands, was significantly shortened from the legs and correlated with spasticity scoring (Ashworth scale). Cortical SEPs from lower limbs were abnormal in all cases, whereas SEPs by stimulation of median nerves were normal; F-wave parameters from upper limbs showed no abnormalities, whereas an increased persistence was detected from lower limbs; H reflex amplitudes resulted larger compared with controls. Moreover, shortening of the CSP, being correlated with the Ashworth scale, can be considered an electrophysiological marker of spasticity that seems to arise from impairment of the supraspinal or intracortical inhibitory pathways with an additional contribution of increased segmental motor neuron excitability. These data prove the existence of comparable neurophysiological abnormalities in ADHSP with spastin mutation (SPG4) when long ascending and descending pathways are involved.     

Abnormalities of parietal and prerolandic somatosensory evoked potentials in Huntington's disease.

Cervical, parietal and prerolandic somatosensory evoked potentials (SEPs) to median nerve stimulation at the wrist were recorded with an earlobe reference in 24 patients with Huntington's disease (HD) and in 24 age-matched normal controls. Cortical responses of abnormal wave form and reduced amplitude were constantly observed in HD patients. SEP changes affected more severely the prerolandic (P22/N30) pattern, which could not be recognized in two-thirds of patients, than the parietal (N20/P27) pattern, which could be identified in all cases. The N20 latency and the central conduction time (N13-N20 interval) were significantly increased. The occurrence of abnormalities of central conduction and of a predominant involvement of the prerolandic SEP pattern suggests an impairment of impulse transmission along the somatosensory lemniscal pathway at subcortical, possibly thalamic, level in HD.     

Somatosensory evoked potentials in lacunar syndromes

Summary Parietal and prerolandic somatosensory evoked potentials (SEPs) to median nerve stimulation were recorded from 40 patients with lacunar syndromes due to CT-verified lacunar infarcts. The control group consisted of 30 age-matched normal controls. Nineteen patients showed SEP abnormalities, mainly an increase of height-covariated latency of cortical components and/or of the central conduction time. Such changes occurred independently of the clinical features of lacunar syndromes, being related more to the lesion location than to its size. SEP studies may be a useful adjunct to the clinical diagnosis of lacunar infarct, possibly also when the CT scans are normal.     

Middle-latency somatosensory evoked potentials after stimulation of the radial and median nerves: component structure and scalp topography.

Somatosensory evoked potentials (SEPs) after radial nerve stimulation are studied less frequently than those after median nerve stimulation. Therefore, little is known about their component structure and scalp topography. We investigated radial nerve SEPs after electrical stimulation at the left wrist. For comparison, the median nerve was also stimulated at the wrist. SEPs were recorded with 15 scalp electrodes (bandpass 0.5-200 Hz) in 27 healthy subjects. The waveform of the radial nerve SEP at a contralateral parietal lead was comparable to that of the median nerve SEP, consisting of P14, N20, P30, and N60. In spite of comparable stimulus intensities, SEP amplitudes were smaller after radial than after median nerve stimulation. Significant latency differences were found only for N20 (earlier for median nerve) and P30 (earlier for radial nerve). The duration of the primary complex N20-P30 thus was significantly shorter for the radial nerve. Whereas N20 and P30 were present with either earlobe or frontal reference, N60 had a prerolandic maximum and was best recorded with a bipolar transverse derivation. In addition, another middle-latency negativity (N110) was found near the secondary somatosensory cortex, which had previously been described only for radial nerve stimulation. In standard SEP derivations, the N110 is riding on the ascending limb of the vertex negativity. It could best be recorded in low temporal leads versus a midline reference. The scalp topographies of P30, N60, and N110 were similar for radial and median nerve stimulation.     

Cerebello-frontal cortical projections in humans studied with the magnetic coil.

Focal stimulation over human cerebellum with a figure 8 magnetic coil (MC) results in an evoked wave recorded from bipolar scalp electrodes on the interaural line and more anteriorly. In 3 subjects, the wave responses along the interaural line had latencies of 8.8-13.8 msec, lasted 17.4-29.0 msec and had a maximum amplitude of 14.4-26.8 microV. The responses were recorded more anteriorly from leads midway between the interaural line and frontal leads; responses recorded from frontal leads were up to 3.5 msec later. The evoked wave was preceded by a diphasic EMG response with a latency of 1.2-2.0 msec. Analysis of the averaged responses recorded by adjoining bipolar leads indicated that the response was predominantly surface positive and crossed. Control experiments eliminated eye movement and somatosensory input as explanations of the evoked response, thereby identifying it as a cortical response. The surface positive wave in humans was compared with the responses recorded in cat and monkey to cerebellar stimulation. The responses in humans could reflect dysfacilitation through MC activation of Purkinje cells, or feed-forward facilitation through transsynaptic or antidromic activation of dentate neurons. The latency of the surface positive wave exceeds that of cerebellar inhibition of MC elicited hand muscle responses, but the discrepancy is at least partly accounted for by the extra delay required to set up the indirect cortico-spinal component required for motoneuron discharge. Estimates made of the cerebello-frontal cortical and peripheral feedback loop times suggest that the central has less than one quarter the delay of the peripheral loop, which would be especially advantageous during fast skilled movements of the fingers.     

The relations between long-latency reflexes in hand muscles, somatosensory evoked potentials and transcranial stimulation of motor tracts

In 15 normal subjects the latency of electrically elicited long-latency reflexes (LLRs) of thenar muscles was compared with somatosensory evoked potentials (SEPs) after median nerve stimulation and with the latencies of thenar muscle potentials after transcranial stimulation (TCS) of the motor cortex. Assuming a transcortical reflex pathway the intracortical relay time for the LLR was calculated to be 10.4 +/- 1.9 msec (mean +/- S.D.) or 8.1 +/- 1.6 msec depending on the experimental conditions. The duration of the cortical relay time is not correlated with the peripheral or central conduction times, with body size or arm length. If the LLRs of hand muscles are conducted transcortically the long duration of the cortical relay time suggests a polysynaptic pathway.     

Somatosensory evoked potentials (SEPs) recorded from deep brain stimulation (DBS) electrodes in the thalamus and subthalamic nucleus (STN).

OBJECTIVE: To examine the location of deep brain stimulation (DBS) electrode somatosensory evoked potentials (SEPs) and determine the generators of the median nerve SEPs recorded in thalamus and subthalamic nucleus (STN). METHODS: SEPs were recorded from contacts of DBS electrodes and microelectrodes in thalamus and STN to establish the latencies of N13, N18 and N20 in 24 patients (8 tremor, 4 chronic pain, 12 Parkinson disease) undergoing chronic DBS. RESULTS: A large SEP with a mean latency of 17.9+/-1.7 ms was recorded from thalamic contacts. Phase reversal occurred at the horizontal level of the anterior commissure-posterior commissure line. Smaller potentials with similar latency but no reversal could be recorded from STN electrodes. CONCLUSIONS: We propose that the thalamic SEP is generated by excitatory post-synaptic potentials in sensory relay neurons in nucleus ventrocaudalis. A small potential in STN at a similar latency, may be due to volume conduction from thalamus. Intraoperative and postoperative SEP recordings from DBS electrodes could be used to determine the optimal position of the contacts relative to the sensory pathways and the choice of contacts for chronic stimulation.     

Short-latency cortical potentials evoked by tactile air-jet stimulation of body and face in man

Natural cutaneous stimulation was performed in 10 healthy volunteers by means of a brief, localized air jet directed to the glabrous skin of the face, finger or toe. Neurograms (from finger stimulation) and somatosensory evoked potentials (SEPs) were recorded and, in the case of finger and toe stimulation, compared with the SEPs obtained by low intensity electrical stimulation. Comparing the latencies at wrist and elbow of the respective neurograms, it appears that a 2 msec period accounts for skin indentation and build-up of the generator potential in the receptors activated by the air jet. A slightly lower conduction velocity was obtained on natural than on electrical stimulation, and the cortical SEPs accordingly had a longer latency. In spite of the much smaller amplitude of the air-jet evoked neurograms, the amplitudes of the SEPs from finger and toe were similar to the amplitudes of the SEPs on electrical stimulation of the same regions. Natural stimulation in the regions innervated by the 3 branches of the trigeminal nerve (tongue included) yielded consistent SEPs, comparable with those reported in the literature to electrical stimulation. These potentials were distinguishable from the electrical activity due to the blink reflex, which invariably takes place on air-jet stimulation of the first trigeminal branch.     

Motor potentials evoked by magnetic stimulation of the motor cortex in normal subjects and patients with motor disorders.

Motor evoked potentials (MEPs) elicited by magnetic coil stimulation of motor cortex were studied at rest and during maximum voluntary muscle contraction in 20 normal subjects and 42 patients with motor disorders. MEP parameters employed in this study included: onset latency, amplitude, MEP/M wave amplitude ratio and background EMG/MEP area ratio. Maximum voluntary contraction increased the amplitude of MEPs compared to the size of M waves elicited by peripheral nerve stimulation. A reduced MEP/M wave amplitude ratio had a higher correlation with pyramidal tract involvement than did a prolonged MEP onset latency. Analysis of MEP parameters may help in the differential diagnosis of cerebral infarction, ALS and cervical spondylotic radiculomyelopathy. The inhibitory period which follows MEPs during voluntary contraction was observed in all subjects; the mean duration in normal subjects was 126.6 +/- 29.5 msec. The mean duration of the inhibitory period in patients with cerebral infarction, ALS and cervical spondylotic radiculomyelopathy was 73.9 +/- 41.7 msec, 79.5 +/- 54.5 msec and 85.1 +/- 36.5 msec, respectively. These values were significantly shorter than in normal subjects.     

Scalp-recorded short and middle latency peroneal somatosensory evoked potentials in normals: comparison with peroneal and median nerve SEPs in patients with unilateral hemispheric lesions

Peroneal somatosensory evoked potentials (SEPs) were performed on 23 normal subjects and 9 selected patients with unilateral hemispheric lesions involving somatosensory pathways. Recording obtained from right and left peroneal nerve (PN) stimulations were compared in all subjects, using open and restricted frequency bandpass filters. Restricted filter (100-3000 Hz) and linked ear reference (A1-A2) enhanced the detection of short latency potentials (P1, P2, N1 with mean peak latency of 17.72, 21.07, 24.09) recorded from scalp electrodes over primary sensory cortex regions. Patients with lesions in the parietal cortex and adjacent subcortical areas demonstrated low amplitude and poorly formed short latency peroneal potentials, and absence of components beyond P3 peak with mean latency of 28.06 msec. In these patients, recordings to right and left median nerve (MN) stimulation showed absence or distorted components subsequent to N1 (N18) potential. These observations suggest that components subsequent to P3 potential in response to PN stimulation, and subsequent to N18 potential in response to MN stimulation, are generated in the parietal cortical regions.     

Long-latency reflexes in contracted hand and foot muscles and their relations to somatosensory evoked potentials and transcranial magnetic stimulation of the motor cortex.

OBJECTIVE: The cortical relay time (CRT) for V2 of long-latency reflexes (LLRs) in the contracted thenar and short toe flexor muscles was studied. METHODS: LLRs and somatosensory evoked potentials (SEPs) were studied by electrical stimulation of the median or posterior tibial nerve. The CRT for V2 was calculated by subtracting the onset latency of cortical potentials in SEPs and that of motor evoked potentials (MEPs) by transcranial magnetic stimulation (TMS) from the onset latency of V2 in eight healthy subjects. RESULTS: The CRT for the thenar muscles was 11.4+/-0.9 ms (mean +/- SD), as the onset latency was 48.8+/-1.4 ms for V2, 16.0+/-1.2 ms for N20 and 21.3+/-1.1 ms for MEP, respectively. The CRT for the short toe flexor muscles was 3.0+/-1.3 ms, as the onset latency was 80.5+/-4.5 ms for V2, 35.3+/-1.8 ms for P38 and 42.2+/-2.0 ms for MEP, respectively. CONCLUSION: Significantly longer CRT for V2 for the thenar muscles (P<0.001, paired Student's t test) may indicate more synaptic relays as compared to that for the short toe flexor muscles.     

Short latency somatosensory evoked potentials to peroneal nerve stimulation: scalp topography and the effect of different frequency filters

Short latency SEPs to peroneal nerve stimulation were recorded from the scalp of 22 normal adults. The scalp topography and the effect of different frequency filters on these potentials were investigated. Using a wider bandpass (5-3000 Hz), this response usually consisted of 3 positive potentials (peak latencies 17, 22 and 27 msec) followed by a negative potential (peak latency 34 msec). Using a narrower bandpass (150-3000 Hz), these potentials were fractionated into subcomponents and up to 6 positive potentials were followed by an often bilobed negative potential occurring 4-10 msec earlier than the first negative potential recorded with the wider bandpass filters. The negative potential and the preceding major positive potentials were well defined and stable within and across normal subjects which suggests they will be useful in the clinical evaluation of patients with spinal cord pathology and in monitoring patients during surgery. Certain of these potentials recorded using the wider bandpass were often characterized by progressive differences in their peak latencies over the scalp. Evidence is provided which suggests that this occurred because subcomponents of these potentials, observed in recordings using the narrower bandpass had different scalp distributions. Evoked potentials were also recorded from surface electrodes placed over the spine of some of these subjects. These recordings when combined with the scalp recordings provided information concerning the conduction characteristics of SEPs from cauda equina to cerebral cortex.     

Motor potentials of inferior orbicularis oculi muscle to transcranial magnetic stimulation. Comparison with responses to electrical peripheral stimulation of facial nerve.

Magnetic stimulation at the vertex evoked a motor potential (MP) in the inferior orbicularis oculi muscle of 10 healthy subjects with an onset latency of 8-13 msec. Its amplitude increased and its latency decreased when the muscle was contracted: the latency measured 9.5 +/- 1.3 msec with an intensity of stimulation 10-15% above threshold in the contracted muscle. This MP is secondary to excitation of the motor cortex. With the coil placed over the occipital scalp and the same stimulation intensity, an MP was recorded with an onset latency at 4.5 +/- 0.6 msec. This response reflects the activation of the facial nerve root. The peripheral electrical stimulation of the facial nerve at the mandible angle elicited an MP with an onset latency at 3.5 +/- 0.4 msec. Most records showed the presence of late components at about 30 msec for all types of stimulation.     

Cortical somatosensory evoked potentials in spinal cord injury patients.

The amplitude and latency of somatosensory evoked potentials (SEPs) in healthy subjects depend on intensity of stimulation. The effect of this parameter on SEPs in patients with neurologic disorders has not been systematically studied, although it could have a profound impact if SEPs are to be used for prognostication. We have compared the latency and amplitude of SEPs in healthy subjects and patients with spinal cord injury (SCI). Stimulation intensity was standardized at two different biologically calibrated levels. Cortical SEPs in patients with SCI showed greater decrease in latency and increase in amplitude with increased intensity of stimulation in comparison to healthy subjects. These phenomena were observed in the majority of patients with incomplete SCI who subsequently showed improvement in cortical SEPs. We observed situations in which the SEP was absent with the usual intensity of stimulation and present only with the stronger stimulation intensity. Furthermore, SEP latencies often changed dramatically with different intensities of stimulation, potentially making any calculation of central conduction velocity meaningless without precise standardization of stimulation. These findings demonstrate a necessity for a biological calibration of stimulation intensity to improve the repeatability of SEPs. We suggest the use of two different standardized intensities of stimulation for SEP studies in SCI patients, one of which should be stronger than the intensity presently recommended.     

Evoked potentials in a man with a complete large myelinated fibre sensory neuropathy below the neck.

Cortical somatosensory evoked potentials (SEPs) were recorded from a man with a severe neuropathy without touch and proprioception below the neck. Peripheral neurophysiological tests showed a complete large myelinated fibre sensory neuropathy. Sensory threshold to electrical stimulation of the median nerve was 15 mA (normal 2-4 mA). With a stimulus of 39 mA, duration 400 microsecons, applied at the wrist a cortical SEP was recorded with a latency of 84 msec, giving a propagation velocity of 11.9 m/sec. At stimulation rates of above 3.3 Hz the SEP was absent. It is concluded that the SEPs recorded were conducted along A delta peripheral fibres.