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.     

Right or left ear reference changes the voltage of frontal and parietal somatosensory evoked potentials.

Short-latency cortical somatosensory evoked potentials (SEPs) to left median nerve stimulation were recorded with either the left or right earlobe as reference. With a right earlobe reference the voltage of the parietal N20 and P27 was reduced while the voltage of the frontal P20 and N30 was enhanced. The effects were consistent, but their size varied with the SEP component considered and also among the subjects. Analysis of SEPs at different scalp sites and at either earlobe suggested that the ear contralateral to the side stimulated picked up transient potential differences, depending a.o. on side asymmetry and geometry of the neural generators as disclosed in topographic mapping. For example, the right ear potential can be shifted negatively by the right N20 field evoked by left median nerve stimulation. The changes involve the absolute potential values, but not the time features or the gradients of potential fields. Scalp current density (SCD) maps are not affected. The results are pertinent for current discussions about which reference to use and document the practical recommendation of recording short-latency cortical SEPs with a reference at the ear ipsilateral (not contralateral) to the side of stimulation.     

Auricular vagus somatosensory evoked potentials in vascular dementia

A new method for the assessment of vagus nerve function has recently been introduced into clinical practice. In the present study we could show that, contrary to our results in Alzheimer’s disease (AD), in patients with vascular dementia (VaD) vagus sensory evoked potentials (VSEP) did not show statistically significant differences as compared to healthy controls. Thus, we hypothesize that the new method of VSEP could possibly contribute to a differential diagnosis between early cases of AD and VaD.     

Somatosensory evoked potentials after removal of somatosensory cortex in man

Somatosensory evoked potentials (SEPs) to median nerve, ulnar nerve, thumb, middle finger, and posterior tibial nerve stimulation were recorded in a patient with a discrete resection of part of the postcentral somatosensory cortex as a treatment for focal epilepsy. Comparison of the different stimulation sites confirmed electrophysiologically the restricted locus of the lesion. The results strongly suggest that the early negative component (N20) and subsequent components recorded postcentrally are of cortical origin and depend upon postcentral gyrus cytoarchitectonic areas 3, 2, and 1. Moreover, these postcentral SEPs are distinct from precentrally recorded activity.     

Short latency somatosensory evoked potentials in patients with neurological lesions

Short latency somatosensory potentials following median nerve stimulation were recorded in patients grouped according to anatomic location of neurological lesion. Patients with cerebral lesions causing severe sensory deficit lacked a major positive wave of cortical origin that in normal subjects peaked at a mean latency of 20.5 ms. Patients with severe cervical spinal cord disease lacked all of the normal somatosensory response except for the earliest component attributed to peripheral nerve activity. Patients with brain-stem lesions showed delayed latencies of later waves and prolonged interwave latencies. However, auditory evoked potentials measured in the group with brain-stem lesions were more helpful in localization. Analysis of short latency somatosensory potentials can discriminate between peripheral nerve, spinal cord, brain-stem, and cerebral lesions. Further experience and refinement of technique of measurement should increase the value of this procedure.     

Short-latency somatosensory evoked potentials in degenerative and vascular dementia.

Short-latency somatosensory evoked potentials (SEPs) were recorded from 54 patients with dementia as compared to 32 age-matched controls. SEPs were generally normal in patients with senile dementia of Alzheimer type, while patients with multi-infarct dementia showed a prolonged central conduction time, an increased latency of both N13 and N20 and a reduction of the primary cortical response amplitude. These findings suggest that recording SEPs may be useful in the differential diagnosis between degenerative dementia and multi-infarct dementia.     

Short-latency somatosensory evoked potentials in infantile autism: evidence of hyperactivity in the right primary somatosensory area

Children with infantile autism sometimes show hyperesthesia or hypoesthesia to touch, pain, and/or temperature. To clarify the pathophysiology, we examined short-latency somatosensory evoked potentials (S-SEPs), elicited by median nerve stimulation, in 24 children with infantile autism (17 males, seven females; age range 2y 2mo-9y; mean age 4y 2mo [SD 1y 7mo]). We also evaluated relationships between S-SEP findings and clinical manifestations. Of the 24 children, 10 showed abnormal S-SEPs as follows: prolonged peak latency of N20 (n=2), extended interpeak latency of P13/14-N20 (n=7), appearance of a giant SEP (n=1), and a more than twofold right hemispheric peak-to-peak amplitude predominance of N20-P25 (n=5). In addition, a peak-to-peak amplitude of N20-P25 elicited by left median nerve stimuli was significantly higher than that obtained with right median nerve stimuli, which indicated right hemispheric hyperactivity relative to the left (p=0.008). Infantile autism is frequently associated with somatosensory abnormalities and right hemispheric hyperactivity relative to the left, especially in the primary somatosensory area. This is believed to contribute to the pathophysiology of infantile autism, especially the idiopathic form.     

Pain-related somatosensory evoked potentials can quantitatively evaluate hypalgesia in Wallenberg's syndrome

In 6 patients with Wallenberg's syndrome who showed a dissociated loss of pain sense, we recorded pain-related somatosensory evoked potentials following CO₂ laser stimulation of the hand dorsum (pain SEPs). Two components, N2 and P2, were recorded by stimulation of the unaffected hand, whereas on the affected side they were absent or decreased in proportion to the severity of hypalgesia which was evaluated by both needle test and CO₂ laser stimulation. Latency of either component, if appeared, was longer in the affected hand stimulation than that in the unaffected one. In contrast, N20 of the conventional electrically-stimulated SEPs (electric SEPs) showed no difference between the two sides. It is concluded that, unlike other electrophysiological methods, pain SEPs following CO₂ laser stimulation can quantitatively evaluate functional impairment of the spinothalamic tract in Wallenberg's syndrome.     

Polysensory evoked potentials in rat parietotemporal cortex: combined auditory and somatosensory responses

A 64 channel microelectrode array was used to map auditory evoked potentials (AEP), somatosensory evoked potentials (SEP) as well as combined auditory and somatosensory evoked potentials (ASEP) from a 7 × mm² area in rat parietotemporal neocortex. Cytochrome oxidase (CO) stained sections of layer IV were obtained in the same animals to provide anatomical information underlying epicortical field potentials. Epicortical responses evoked by click or vibrissa stimuli replicated earlier findings from our laboratory, and appeared as a family of waveforms centered on primary auditory (AI) or somatosensory (SI) cortical areas as determined from CO histology. Selective microinjections of HRP to AI and SI further confirmed their specific sensory relay nuclei in the thalamus. A small polysensory area between AI and SI, responded uniquely with an enhanced negative sharp wave to combined auditory and somatosensory stimuli. HRP retrograde labeling revealed that the thalamocortical projections to this area were from the posterior nuclear group (Po) and medial division of the medial geniculate (MGm). These data establish close relationships between epicortical AEP, SEP, and especially ASEP and corresponding cortical structures and thalamocortical projections. The neurogenesis of unimodal and polysensory evoked potentials is discussed in terms of specific and non-specific systems.     

脊椎旁刺激法体感诱发电位在脊髓病变中的临床应用

目的 探讨脊椎旁刺激法体感诱发电位（SEPs）在脊髓病变患者中进行脊髓功能判断的临床应用价值，并将诱发电位结果与脊髓MRI结果进行比较，初步探讨该方法在脊髓病变中的生理定位价值。方法 应用脊椎旁刺激、头皮记录的直接SEPs法对脊髓病变患者进行SEPs测定及脊髓传导速度（SCCV）测定。结果 共有96例脊髓病变患者行脊椎旁刺激法SEPs及SCCV测定，男53例，女43例，年龄15-75岁，平均46．78岁。其中脊髓脱髓鞘病36例，脊髓亚急性联合变性26例，脊髓病19例，急性脊髓炎10例，脊髓压迫性疾病5例。96例脊髓病变患者均做脊椎旁刺激法SEPs检查，脊髓诱发电位及SCCV的异常率在各脊髓病变中阳性率均较高，总异常率为81．25％（78／96）。其中脊髓脱髓鞘病异常率75．00％（27／36），脊髓亚急性联合变性异常率88．46％（23／26），脊髓病19例中有15例异常，脊髓炎异常率10例中有8例异常，脊髓压迫症5例均异常。共有68例患者做脊髓MRI检查，其中42例MRI异常，26例MRI正常。42例MRI异常患者中35例诱发电位结果异常，26例MRI正常患者中21例诱发电位结果异常。结论 脊椎旁刺激法SEPs及SCCV的测定客观地记录了脊髓病变的异常电生理改变，其异常电生理改变可能会出现在脊髓结构改变及影像学改变之前，可为脊髓病变患者早期脊髓功能性改变提供比较可靠的客观诊断依据，尤其在脊髓MRI少有阳性所见的营养代谢性脊髓病中意义更大。本方法简单、无创、具有可重复性，可在临床中应用。     

Extreme somatosensory evoked potentials (ESEPs) elicited by tapping of hands or feet in children: a somatosensory cerebral evoked potentials study

Six children with tactile-evoked spikes in the EEG, also defined as extreme somatosensory evoked potentials (ESEPs), underwent an SEPs study in order to define the characteristics of such evoked potentials. Short-latency SEPs showed normal mean latency and amplitude values. Mid- or long-latency SEPs of abnormally high amplitude were recorded after stimulation of one or more extremities. Such extreme responses which showed the same reactivity proper to normal long-latency SEPs could be considered to correspond to the evoked spikes in the EEG.     

Short-latency somatosensory evoked potentials in myotonic dystrophy: evidence for a conduction disturbance

Short-latency somatosensory evoked potentials were recorded in 13 patients with myotonic dystrophy (MyD). The MyD were compared with age-matched controls. The mean conduction latency between the brachial plexus and dorsal column nuclei (EP-N14) was significantly longer for the MyD. Results suggest an afferent conduction disturbance in MyD.     

Role of somatosensory evoked potentials in the diagnosis of peripheral nerve lesions: recent advances

Short-latency somatosensory evoked potentials (SEPs) have become an important tool in the investigation of peripheral nerve lesions. Electrically evoked SEPs are most suitable because they provide results with small variations and are readily repeatable. Techniques for testing 10 different upper and lower limb nerves, dermatomes, cutaneous fibers of trigeminal nerve, and nerves supplying urogenital areas are now available. The established, principal areas of application are in the investigation of brachial plexus lesions, proximal injuries of individual nerves in upper and lower limbs, and painful dysesthesias and in the differential diagnosis of pain caused by psychogenic causes or organic lesions. The techniques have proven to be of value in demonstrating early proximal abnormalities in polyneuropathies. Abnormalities have occurred in trigeminal nerve lesions, urogenital dysfunctions, hereditary ataxias, and rare neuropathies. Unexpected abnormalities have also been reported in motor neuron disease, myotonic muscular dystrophies, and other conditions. Applications in the diagnosis of spondylopathic root lesions are not satisfactory; the techniques' usefulness in the investigation of these lesions does not extend beyond aiding the selection of patients for other diagnostic modalities, such as myelography, computed tomography (CT), and nuclear magnetic resonance (NMR) imaging. The usefulness of SEP techniques in the diagnosis of peripheral nerve lesions will remain, even if advances in organ imaging techniques can provide more specific information about the level and magnitude of lesions in the central nervous system. SEP techniques are an important complement to the other well-established methods, such as clinical testing, electromyography, and nerve conduction studies.     

Superior colliculus lesions and flash evoked potentials from rat cortex

It is generally assumed that the primary response of the rat flash evoked potential (FEP) is activated by a retino-geniculate path, and that the secondary response reflects input to the cortex by way of the superior colliculus (SC) or other brainstem structures. In the present study, male Long-Evans rats were implanted with monopolar screw electrodes placed over the left visual cortex, and a pair of twisted monopolar depth electrodes, which were used to produce electrolytic lesions, were placed in each SC. One half of the animals did not receive the electrolytic treatment (controls). FEP waveforms were obtained from all animals prior to treatment, and 2 and 5 days after treatment. Histological analysis was performed to verify electrode placement and determine lesion size. Electrolytic lesions resulting in massive destruction of the SC produced no decrement in any portion of the rat FEP but did produce an increase in amplitude of the N2P3 component. The data show that the secondary response is not generated by SC in rats, but that SC may modulate amplitude of the response.     

Frontal and parietal components of enhanced somatosensory evoked potentials: a comparison between pathological and pharmacologically induced conditions

Pathologically enhanced somatosensory evoked potentials (giant SEPs) were recorded in 10 patients with cortical myoclonus of various origins. With non-cephalic reference electrodes a giant frontal negativity corresponding to normal N30 was found over the contra- and ipsilateral hemispheres which was not simply a phase reversal of the well-known enhanced parietal P25. The preceding far-field P14, parietal N20 and frontal P22 were of normal size. A similar result was found when SEPs were studied during the action of etomidate, an ultrashort-acting non-barbiturate hypnotic which produced a marked increase of the parietal P25 and frontal N30 after intravenous administration. These increased components, on the other hand, were abolished when recording was repeated immediately after application of electroconvulsive shock whereas P14, N20, and P22 remained more or less unchanged in both conditions. Our results indicate that there are neuronal elements in the sensorimotor cortex which are more resistant to influences such as narcotic drugs and seizure activity than others, being highly modifiable by these alterations. It is speculated whether these highly modifiable cortical systems are those in which giant SEPs, as well as pharmacologically increased SEP components, arise.     

Giant somatosensory evoked potentials in the Rett syndrome

Somatosensory evoked potentials (SEP) were recorded in ten patients with the Rett syndrome. Seven cases showed abnormal SEP, and five of these cases showed giant SEP. The five cases with giant SEP were relatively young girls with epilepsy and parieto-central spikes on the electro-encephalogram (EEG). Older patients did not show giant SEP. These giant SEP may be the reflection of cortical hyperexcitability and they may subside as the disease progresses.     

Interhemispheric transmission: assessment with vibratory somatosensory evoked potentials

Interhemispheric transmission time (ITT) was derived from vibratory somatosensory evoked potentials (VSEP) arising in homologous cortical sensory--association areas of normals. Two different vibratory sources, an audiometer bone oscillator or an Optacon, were used to stimulate each index finger independently. ITT was calculated by subtracting the latency of the first major peak over the contralateral cortex (CL) from the latency of the corresponding peak over the ipsilateral area (IL-CL = ITT). Readily identified aberrant values were observed and rejected from the series of measurements leaving clear normal ranges. In addition to providing normal ITT data, clinical correlations were illustrated in two different disorders. Results suggested that important information relating to diagnosis and therapy of brain pathologies affecting interhemispheric transmission can now be made available in both experimental and clinical situations.