Origin of the widespread N18 in median nerve SEP

The widespread N18 potential in median nerve SEP was studied in normal subjects and in patients with high cervical, brain-stem and thalamic lesions who had profound disturbances of deep sensation. N18 was well identified in the HSi-CV2 derivation in every normal subject as a broad elevation from the baseline lasting about 20 msec. The cortical N20 was absent in all patients. N18 was absent in a patient with a dorsal column lesion at C1-2 level. The amplitude and configuration of N18 were normal in all other patients with brain-stem and thalamic lesions, including a patient with a lesion at the ponto-medullary junction. The sagittal distribution of N18 was studied in a patient with a thalamic lesion and an oblique distribution with the maximum region between Cz and nasion was demonstrated. The present results indicate that at least the greater part of N18 is generated at the caudalmost brain-stem or through branches from this level. Taking previous animal and intraoperative studies into consideration, we think it most probable that the main part of N18 corresponds to the ventro-rostral negative pole of the dipolar potential generated at the cuneate nucleus by the primary afferent depolarization of presynaptic terminals of dorsal column fibers.     

Topography of somatosensory evoked potentials to median nerve stimulation in patients with cerebral lesions

Scalp distributions and topographies of early cortical somatosensory evoked potentials (SEPs) to median nerve stimulation were studied in 22 patients with 5 different types of cerebral lesion due to cerebrovascular disease or tumor (thalamic, postcentral subcortical, precentral subcortical, diffuse subcortical and parieto-occipital lesions) in order to investigate the origins of frontal (P20, N24) and central-parietal SEPs (N20, P22, P23).In 2 patients with thalamic syndrome, N16 was delayed in latency and N20/P20 were not recorded. No early SEP except for N16 was recorded in 2 patients with pure hemisensory loss due to postcentral subcortical lesion. In all 11 patients with pure hemiparesis or hemiplegia due to precentral subcortical lesion N20/P20 and P22, P23/N24 components were of normal peak latencies. The amplitude of N24 was significantly decreased in all 3 patients with complete hemiplegia. These findings support the hypothesis that N20/P20 are generated as a horizontal dipole in the central sulcus (3b), whereas P23/N24 are a reflection of multiple generators in pre- and post-rolandic fissures. P22 was very localized in the central area contralateral to the stimulation.Topographical studies of early cortical SEPs are useful for detecting each component in abnormal SEPs     

Latency and amplitude abnormalities of the scalp far-field P14 to median nerve stimulation in multiple sclerosis. A SEP study of 122 patients recorded with a non-cephalic reference montage

The frequency and characteristics of P14 abnormalities were investigated in 122 patients with probable (68), or definite (54) multiple sclerosis by recording SEPs to median nerve stimulation with a non-cephalic reference montage. The most frequent SEP abnormality found in our series (62% of abnormal results) combined latency increase and amplitude reduction of P14. Interindividual variability, inherent in absolute amplitude measurements, was by-passed by calculating the ration between the amplitudes of far-field P9 and P14 components, which proved to be normally distributed in controls. In spite of the strong association (P ⪡ 0.001) between the P9–P14 interpeak interval (IPL) and the P9/P14 amplitude ratio in MS patients, the latter parameter was found to be the only abnormality in 12 patients whose P9–P14 and P14–N20 IPLs were normal. Also IPLs were increased in 12 patients with normal P14 amplitudes. These results suggest that adding the P9/P14 amplitude criterion to standard IPL data might be useful to detect conduction troubles in MS patients.     

Origin of frontal N15 component of somatosensory evoked potential in man

Origin of the frontal somatosensory evoked potential (SEP) by median nerve stimulation was investigated in normal volunteers and in patients with localized cerebrovascular diseases, and the following results were obtained.

• 1.(1) In normal subjects, SEPs recorded at F3 (or F4) contralateral to the stimulating median nerve were composed of P12, N15, P18.5 and N26. Similar components were recognized in SEP recorded at Fz.
• 2.(2) In patients in whom putaminal or thalamic hemorrhages had destroyed the posterior limbs of the internal capsules, frontal N15 and parietal N18 (N20) disappeared. These components were also absent in patients with cortical (parietal) infarctions. Among these patients, the thalamus was not affected in cases with putaminal hemorrhages and cortical infarctions.

These facts indicate that the generator of the frontal N15 does not exist in the thalamus but that it originates from the neural structure central to the internal capsule, which suggests a similarity to the generator of the parietal N18.Because N15 was recorded in the midline of the frontal region with shorter latency than parietal N18, the frontal N15 might represent a response to the sensory input of the frontal lobe via the non-specific sensory system.     

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.     

Brain-stem somatosensory dysfunction in a case of long-standing left hemispherectomy with removal of the left thalamus: a nasopharyngeal and scalp SEP study

We have studied median nerve somatosensory evoked potentials (SEPs) in a patient who had undergone early surgical removal of the left cerebral hemisphere and left thalamus. Stimulation of the right side evoked normal latency P9, P11 and P13 potentials at scalp as well as at nasopharyngeal (NP) leads, while P14 and N18 potentials were absent. These SEP abnormalities, that have been described previously in cervico-medullary lesions and in comatose patients with upper brain-stem involvement, suggest that in our patient the removal of the left thalamus has caused retrograde degeneration of the cuneate-thalamic projections. Moreover, this study confirms that P13 and P14 potentials have different generators.     

Clinical and neuroimaging correlates of abnormal short-latency Somatosensory Evoked Potentials in elderly vascular dementia patients: A psychophysiological exploratory study

BACKGROUND: Short Latency Somatosensory Evoked Potentials (SEPs) may serve to the testing of the somatosensory tract function, which is vulnerable and affected in vascular encephalopathy. The aim of the current study was to search for clinical and neuroimaging correlates of abnormal SEPs in vascular dementia (VD) patients. MATERIALS AND METHODS: The study included 14 VD patients, aged 72.93 PlusMinus; 4.73 years, and 10 controls aged 71.20 PlusMinus; 4.44 years. All subjects underwent a detailed clinical examination, blood and biochemical testing, brain MRI and were assessed with the MMSE. SEPs were recorded after stimulation from upper and lower limbs. The statistical Analysis included 1 and 2-way MANCOVAs and Factor analysis RESULTS: The N13 latency was significantly prolonged, the N19 amplitude was lower, the P27 amplitude was lower and the N11-P27 conduction time was prolonged in severely demented patients in comparison to controls. The N19 latency was prolonged in severely demented patients in comparison to both mildly demented and controls. The same was true for the N13-N19 conduction time, and for the P27 latency. Patients with subcortical lesions had all their latencies prolonged and lower P27 amplitude. DISCUSSION: The results of the current study suggest that there are significant differences between patients suffering from VD and healthy controls in SEPs, but these are detectable only when dementia is severe or there are lesions located in the subcortical regions. The results of the current study locate the abnormal SEPs in the white matter, and are in accord with the literature.     

γ-氨基丁酸、荷包牡丹碱和L-谷氨酸钠对猫和家兔同侧和对侧图形视觉诱发电位的影响

在猫和家兔大脑半球一侧视区17/18交界处施加γ—氨基丁酸(GABA)、荷包牡丹碱和L—谷氨酸钠,以及用氯化钾和冷冻阻遏的方法,记录对侧和同侧皮层相应处图形视觉诱发电位(PVEP)的变化。讨论了GABA、荷包牡丹碱和L—谷氨酸钠对猫和兔的对侧和同侧PVEP的影响。     

Intracranial recording of short latency somatosensory evoked potentials in man: Identification of origin of each component

In normal subjects the short latency SEPs generally consisted of 3 positive waves (P9, P11, P14) and a succeeding negative wave (N20). To determine the origins of these waves we have made intracranial records from 17 patients, which suggest the following results. P9 originates in stimulated median nerve peripheral to the dorsal roots such as brachial plexus, P11 in the dorsal column of the cervical cord, P14 in the cuneate nucleus and medial lemniscal pathway, and N20 in the cerebral cortex. On the basis of intracranial and intraspinal records, the onset of P11 indicates the arrival of the afferent volley at the cord entry and the peak latency of P11 its arrival time at the C1–2 level dorsal column. The onset latency of P14 indicates the onset of postsynaptic events in cuneate nucleus neurons and the peak latency of P14 arrival at the midbrain.From the ventral surface of the brain-stem 3 positive waves (P′9, P′11, P′14) like the initial positive components of the scalp short latency SEPs (P9, P11, P14) were recorded. The amplitude of P′14 was large compared to that of P14. The peak latencies of P′14 recorded at the medulla and the pons were shorter than that of P14 by 0.7–0.8 msec and 0.2–0.5 msec, respectively. The peak latency of P′14 at the midbrain was almost the same as that of P14. By measuring the distance between the recording electrodes in the brain-stem and the peak latency difference of P′14, the fastest lemniscal conduction velocity was estimated as 56 m/sec.     

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.     

Short-latency somatosensory evoked potentials following median nerve stimulation in Down's syndrome

Short-latency somatosensory evoked potentials (SEPs) following median nerve stimulation were recorded in 42 patients with Down's syndrome and in 42 age- and sex-matched normal subjects. There were no significant differences between the 2 groups in the absolute peak latencies of N9, N11 and N13 components. However, interpeak latencies, N9-N11, N11-N13 and N9-N13, were prolonged significantly in Down's syndrome. These findings suggest impaired impulse conduction in the proximal part of the brachial plexus, posterior roots and/or posterior column-medial lemniscal pathway. Interpeak latency N13-N20, representing conduction time from cervical cord to sensory cortex, was not significantly different between the 2 groups. Cortical potentials N20 and P25 in the parietal area and P20 and N25 in the frontal area were of significantly larger amplitude in Down's syndrome. P25 had double peaks in 16 of 42 normal subjects, but these were not apparent in any of the patients.     

SEPs in two patients with localized lesions of the postcentral gyrus

Scalp distributions of median nerve SEPs were studied in normal controls and 2 patients with localized lesions of the postcentral gyrus. In controls, parieto-occipital electrodes registered N20-P27 while frontal electrodes registered P20-N27. Other small components, parieto-occipital P22 and frontal N22, were recognized in about half of the control records. The wave forms at a frontal and a parieto-occipital electrode, both distant from the central region, formed exact mirror images of each other concerning N20-(P22)-P27 and P20-(N22)-N27. Electrodes near the central region contralateral to the stimulation registered cP22-cN30 (central P22 and central N30). When the postcentral gyrus was damaged, N20/P20-P27/N27 and cP22-cN30 were eliminated and the only remaining components were a frontal negative wave (frN) and a contralateral parieto-occipital positive wave (poP). Digital nerve stimulation also evoked poP and frN in both cases. In case 2, poP coincided with P22 of the non-affected side. The following generators were proposed; N20/P20-P27/N27: area 3b, cP22-cN30: areas 1 and 2, poP/early frN (= P22/N22): area 4 at the anterior wall of the central sulcus (due to direct thalamic inputs to motor cortex), late frN: uncertain (SMA?, SII?).     

The Use of Neutral Lipid Fatty Acids to Indicate the Physiological Conditions of Soil Fungi

The usefulness of measuring neutral lipid fatty acids (NLFAs) and phospholipid fatty acids (PLFAs) separately in order to interpret perturbation effects on soil and compost microorganisms has been studied. Initially the NLFA/PLFA ratios were studied in different soils. Low ratios were found for fatty acids common in bacteria, especially for cyclopropane fatty acids. Higher ratios were found for fatty acids common in eukaryotic organisms such as fungi (18:1omega9 and 18:2omega6,9) or in saturated fatty acids, common to many types of organisms. Adding glucose to a forest soil increased the amounts of the fungal NLFAs 18:1omega9 and 18:2 omega6,9 up to 60 and 10 times, respectively, after 10 days, followed by a gradual decrease. After 3 months incubation, higher levels of these NLFAs were still found compared with the control samples. Adding glucose together with nitrogen (N) and phosphorus (P) resulted in no increase in NLFAs but a 10-fold increase in the PLFAs 18:1omega9 and 18:2omega6,9. Thus, the NLFA/PLFA ratios for these fatty acids were lower than in the no-addition control when glucose was added together with N and P, but higher when glucose was added alone, even 3 months after the addition. Adding N+P without glucose did not affect the NLFA/PLFA ratio for any fatty acid. Increasing NLFA/PLFA ratios for the fungal fatty acids were also found with time after the thermophilic phase in a compost, indicating increased availability of easily available carbon.     

Median nerve somatosensory evoked potentials. Apomorphine-induced transient potentiation of frontal components Clin. Parkinson's disease and in parkinsonism

Somatosensory evoked potentials (SEPs) to median nerve stimulation have been recorded from parietal and frontal districts Clin. 43 parkinsonians, 17 patients with parkinsonism and 35 healthy controls matched for age and sex. Latency/ amplitude characteristics of the parietal P14-N20-P25 and of the frontal P20-N30-P40 wave complexes before and after (10, 20, 30 and 60 min) subcutaneous administration of apomorphine chloride were evaluated Clin. all the 60 patients and Clin. 3 controls. The frontal waves N30 and P40 were either absent or significantly smaller than normal Clin. 31 patients with Parkinson's disease (PD) (72.1%) and Clin. 9 with parkinsonism Clin. baseline records (56.3%). Following apomorphine, the parietal deflections did not significantly vary Clin. amplitude. On the contrary, the frontal complex showed a significant amplitude increase Clin. 27 PD and 8 parkinsonisms (respectively 62.8 and 47.1%): 79.1% of PD and 35.3% of parkinsonisms were improved clinically. Amplitude increase was evident at 10 min after apomorphine, Clin. parallel with clinical improvement, and vanished nearly Clin. coincidence with the end of the clinical effect.     

The N18 component of the median nerve SEP is not reduced by vibration

Objective: To study the interference of mechanical vibration of the palm of the hand on the median nerve short-latency SEP components.Methods: Electrically-elicited short-latency median nerve SEP were obtained before and during mechanical vibration (120 Hz) of the palm in two groups of normal individuals (6 in group I and 9 in group II). The amplitude of the different components was compared between the two conditions through non-parametric statistical tests.Results: A significant reduction in the amplitude of the N9, P13/14 and N20 components was detected, however no overall significant changes were detected for the N18 component.Conclusions: Vibration interference reduced all studied components except the N18, these findings are interpreted as supporting evidence for the proposed association between the N18 component and the inhibitory activities elicited in the dorsal column nuclei.     

Detailed analysis of the latencies of median nerve somatosensory evoked potential components, 2: analysis of subcomponents of the P13/14 and N20 potentials

Detailed analysis of P13/14 and N20 wavelets was performed for 62 normal subjects and patients with various lesions along the somatosensory pathway. A histogram of the latencies of all the identified P13/14 wavelets (measured from P13/14 onset) demonstrated three latency-groups, which were named P13, P14a and P14b subcomponents. The relationship between the three newly identified subcomponents and the conventional naming of P13 and P14 was inconstant, indicating the ambiguity of the latter. P14b was most prominent in the contralateral central region, and therefore a P15 positivity slightly after P14b was often recorded in the CPc-Fz and CPc-CPi leads (CPc and CPi are centroparietal electrodes contralateral and ipsilateral to the stimulation). P14b/P15 was lost even in patients with cortical lesions, and thalamocortical fibers were assumed for its origin. The CPc-Fz and CPi-Fz leads registered a low negativity named broad N13', suggesting frontal predominance of the overall P13/14 complex. Both P13 and P14a were identified in a patient with a pontine lesion, and a caudal brainstem origin for both was suspected due to the onset of two repetitive bursts of the ascending lemniscal volley. We refuted the presynaptic origin of the scalp P13 potential and pointed out that a prolonged and/or polyphasic P11 frequently observed in patients with high cervical lesions can be mistaken as scalp P13. A histogram of the latencies of all the identified negative wavelets of N20 in the CPc-Fz lead (measured from N20 onset) revealed five definite latency-groups, which were named N20a, N20b, N20c, N20d and N20e subcomponents. The highest peak of N20 actually corresponded to either N20b, N20c or N20d, and this uncertainty, which must be related to intracortical processes, resulted in a large instability of the N20 peak latency as well as the age and sex dependence of the N20 onset-peak interval, both of which were demonstrated by our preceding study (Sonoo, M., Kobayashi, M., Genba-Shimizu, K., Mannen, T. and Shimizu, T. Detailed analysis of the latencies of median nerve SEP components, 1: selection of the best standard parameters and the establishment of the normal values. Electroenceph. clin. Neurophysiol., 1996b, 100: 319–331). Negative subcomponents in the CPc-NC lead and positive subcomponents in the Fz-NC lead constituted mirror images of each other, which suggested that these subcomponents were generated within area 3b.     

Comparison in man of short latency averaged evoked potentials recorded in thalamic and scalp hand zones of representation

Recordings were performed in the thalamus of 13 patients suffering from either abnormal movements or intractable pain, with the aim of delimiting the region to be destroyed or stimulated in order to diminish the syndrome. In 11 of these patients averaged evoked potentials were recorded simultaneously from the scalp and specific thalamus (VP) hand area levels following median nerve stimulation. These recordings were done during the operation or afterwards when an electrode was left in place for a program of stimulation.The latencies of onsets and peaks on the scalp ‘P15’ were compared with those of the VP wave; a clear correspondence was found. Moreover, when increased stimulation was used, both waves began to develop in parallel. Thus in the contralateral ‘P15’ a component exists due to the field produced by the thalamic response. To explain the presence of an ipsilateral scalp ‘P15’ wave, we propose that a second wave having the same latency and a slightly shorter peak exists on the scalp due to a field produced by a brain-stem response. This double origin of ‘P15’ is also shown by the different changes which the ipsilateral and contralateral waves present during changes in alertness.The scalp ‘N18–N20’ is also composed of at least 2 components. The first peak appears on the scalp with a latency shorter than that of the negativity which develops in the thalamus. The N wave, moreover, increases in latency with rapid stimulus repetition. We propose with others that ‘N18’ is a cortical event reflecting the arrival of the thalamo-cortical volley. The second component, ‘N20,’ has a peak latency closely correlated to that of the thalamic negativity. This component was present alone in ‘N’ when rapid stimulation (> 4/sec) was used, which did not change the thalamic response. It must be a field produced by the thalamic negativity.     

Origin and distribution of P13 and P14 far-field potentials after median nerve stimulation. Scalp,nasopharyngeal and neck recording in healthy subjects and in patients with cervical and cervico-medullary lesions

We studied median nerve SEPs in 10 healthy subjects, by means of simultaneous recording over the scalp, around the neck and near the ventral surface of the medulla using a nasopharyngeal (NP) electrode. This recording technique enabled us to clearly differentiate P13 and P14 potentials. The former was always found in NP records, while the latter was more evident in scalp traces. The same technique was used to study 9 patients with various lesions of the cervical cord or cervico-medullary junction. Patients with high cervical lesions demonstrated abnormalities of both P13 and P14 potentials, while patients with lesions of the cervico-medullary junction demonstrated a clear dissociation between normal P13 in scalp and NP traces, and abnormal scalp P14. Patients with lower cervical lesions, selectively involving the central grey matter, showed normal P13 and P14 potentials, in spite of abnormal N13 cervical responses. Our findings strongly suggest that both scalp and NP P13 have the same generators in higher segments of the cervical cord, and that NP more than scalp records are effective in analyzing the P13 response. We suggest that the selective recording of the P13 potential could be useful in the assessment of focal lesions of the higher cervical cord or of the cervico-medullary junction.     

Growth hormone and carbohydrate intolerance in cirrhosis

Patients with cirrhosis of the liver often have insulin resistance and elevated circulating growth hormone levels. This study was undertaken (a) to evaluate glucose intolerance, insulin resistance and abnormal growth hormone secretion and (b) to determine if GH suppression improves insulin resistance. Glucose tolerance tests (GTT), intravenous insulin tolerance tests (IVITT), arginine stimulation tests (AST) and glucose clamp studies before and during GH suppression with somatostatin were performed in a group of patients with alcohol-induced liver cirrhosis. During GTT cirrhotic subjects had a 2-hour plasma glucose of 200 +/- 9.8 ng/dl (N = 14) compared to 128 +/- 8.0 ng/dl in normal controls (N = 15), P less than 0.001. Basal GH was elevated in cirrhotic patients and in response to arginine stimulation reached a peak of 17.0 +/- 5.4 ng/ml (N = 7), compared to a peak of 11.3 +/- 1.8 ng/ml in 5 normal controls (P = NS). During IVITT patients with cirrhosis had a glucose nadir of 60.0 +/- 4.0 mg/dl (N = 9), compared to 29.0 +/- 7.0 mg/dl in controls (N = 5), P less than 0.001. Peak GH levels during IVITT were not significantly different in cirrhotics and controls. Glucose utilization rates in 4 patients with cirrhosis of the liver before somatostatin mediated GH suppression was 3.1 +/- 0.5 mg/kg/min and 6.5 +/- 1.5 mg/kg/min during somatostatin infusion, P less than 0.025. We conclude that patients with alcohol induced cirrhosis have sustained GH elevations resulting in insulin resistance which improves after GH suppression.     

Interocular interaction assessed by VEPs to pattern-onset, -reversal,and -offset in normally sighted and amblyopic subjects

The extent of interocular interaction reflected in sequentially averaged VEPs to checkerboard onset, reversal and offset stimulation was investigated to assess the relative efficacy of the three modes of pattern stimulation. Thirty-one controls and 18 amblyopic children were studied. Components on the side of the scalp ipsilateral and contralateral to the stimulated left half-field were measured for checksizes 12′, 20′, 50′ and 80′. Binocular:monocular amplitude ratios for normals were compared with `binocular:good eye' amplitude ratios for amblyopes. The reversal P100 ratio was found to differ significantly between normals and amblyopes for 12′, 20′ and 50′ checks. Ipsilateral (CII) and contralateral (P105) onset components also differed significantly but for the smallest 12′ checks only. In controls, onset components (P105 and CIII) and, reversal components (N80 and P100) showed significantly shorter binocular as compared with monocular latencies. These latency differences were not found in amblyopes. Our results show that interocular interaction in normals is best shown by potentials which predominantly reflect macular pathway activation, and are most conspicuous for reversal N80 and P100 components. Similarly, these components demonstrated the clearest differences when comparing binocular interaction effects between controls and amblyopic subjects.