Spinal somatosensory evoked potentials in hereditary spastic paraplegia.

Cervical somatosensory evoked potentials elicited by median nerve stimulation were recorded from 18 cases of hereditary spastic paraplegia. Motor and sensory nerve conduction in the median nerve was normal in each. In one third of the patients no spinal evoked potential was detectable. In the remainder the amplitude of the evoked potential was reduced in comparison with a control series; the latency was not significantly different. These changes suggest that a selective degeneration of the centrally directed axons derived from the dorsal root ganglion cells occurs in this disorder. The findings are discussed in relation to previous reports on the pathological appearances.     

Subcortical and cortical somatosensory potentials evoked by posterior tibial nerve stimulation: normative values

Cortical somatosensory evoked potentials to posterior tibial nerve stimulation were obtained in 29 normal controls varying in age and body height. In obtaining these potentials we varied recording derivations and frequency settings. Our recordings demonstrated the following points: N20 (dorsal cord potential) and the early cortical components (P2, N2) were the only potentials that were consistently recorded. All other subcortical components (N18, N24, P27, N30) were of relatively low amplitude and not infrequently absent even in normals. All absolute latencies other than N2 were correlated with body height. However, interpeak latency differences were independent of body height. Below the age of 20, subcortical but not cortical peak latencies correlated with age, but this appeared to be due to changes in body height in this age group. Absolute amplitudes and amplitude ratios (left/right and uni/bilateral) showed marked interindividual variability and have very limited value in defining abnormality. The use of restricted filter windows facilitated the selective recording of postsynaptic potentials (30-250 Hz) and action potentials (150-1500 Hz).     

Estimation of cervical cord dysfunction by somatosensory evoked potentials

The purpose of this study was to examine the relationship of abnormal short-latency somatosensory evoked potentials (SSEPs) recorded by a noncephalic reference montage with clinical variables in cervical myelopathy patients and to reexamine the diagnostic utility of SSEPs in such patients. We studied cervical SSEPs elicited by stimulating the median and ulnar nerves in 87 patients. Our grade classification of spinal N13, which is based on the normal limits of latencies or amplitudes, corresponded well with the clinical variables and is of value when trying to localize the cervical lesion segmentally. The N9-P14 interpeak latency in response to ulnar nerve stimulation correlated well with lower extremity function (r = -0.440, P <0.0001). We suggest a combined assessment of N13 amplitude, and N9-N13 and N9-P14 interpeak latencies to estimate dorsal column and dorsal horn function separately in patients with cervical myelopathy.     

Multimodality evoked potentials in amyotrophic lateral sclerosis

Visual, brainstem auditory and somatosensory evoked potentials to medial nerve stimulation were recorded in 27 patients affected by amyotrophic lateral sclerosis. VEP N75, P100, N140, N75-P100 latencies and P100 amplitude, BAEP I-III, III-V and I-V interpeak-latencies were within normal limits in all ALS patients. Somatosensory evoked potentials were abnormally delayed in 8 patients: in 3 arms because of a delayed N9-N13 latency, in 9 arms because of a delayed N13-N19 latency.     

Strümpell's familial spastic paraplegia: an electrophysiological demonstration of selective central distal axonopathy

Three patients with autosomal dominant Strümpell's familial spastic paraplegia (SFSP) were evaluated by means of somatosensory evoked potentials (SEPs) from upper and lower limb and determination of sural nerve conduction velocity. Findings of normal sural nerve conduction but reduced amplitude and poor definition of SEPs with normal latencies on peroneal nerve stimulation support a pattern of central nervous system degeneration characterized by a selective involvement of centrally directed axons within the gracile fasciculi.     

Visual and somatosensory evoked potentials characteristics of patients undergoing hemodialysis and kidney transplantation.

The effects of prolonged hemodialysis and kidney transplantation on visual and somatosensory evoked potentials and EEG frequency were assessed. Significant changes were found in both amplitude and latency characteristics of evoked potentials recorded from eight hemodialysis patients. Their evoked potentials tended to be of longer latency and larger amplitude when compared to responses of an age-matched control group. This was true for visual and somatosensory responses recorded from several scalp locations. A correlational analysis revealed no consistent relationship between blood chemistries and evoked potential characteristics. EEG power spectral analysis showed that the dominant frequency of five of the eight dialysis patients was in the 8-10 c/sec range. Two other patients demonstrated EEG frequencies which were scattered across the 3-12 c/sec range while for another subject the dominant frequency was 7-8 c/sec. The evoked potential latencies and amplitudes of patients with successful kidney transplant tended to return to the normal range and their predominant EEG frequency increased to around 10 c/sec. A depression of function in those neural systems underlying the visual and somatosensory modalities, along with a reduction in the cortical suppression of afferent stimulation normally exerted by the thalamic reticular system and the basal ganglia were postulated to account for the reported findings.     

The N30 component of somatosensory evoked potentials in patients with dystonia.

We recorded short-latency median nerve somatosensory evoked potentials (SEPs) in 10 patients with dystonia (6 with focal dystonia, 3 with generalized dystonia, and 1 with segmental dystonia) and compared them with those of 10 normal controls. The EEG was recorded from 29 sites on the scalp with linked earlobe electrodes for reference. Latencies and amplitudes of P15, postcentral N20 and P45, and frontal N30 were evaluated. The latencies of all potentials were the same in patients and controls. The amplitudes of P15, N20 and P45 were also the same in both groups, but the N30 amplitude of the patients was larger than of the controls. The amplitude of N30 did not vary from the affected side to the unaffected side. Previous work has shown decreased N30 amplitude in patients with Parkinson's disease. Changes in N30 amplitude may be indicative of abnormal excitatory effects on cortex resulting from disorders of the basal ganglia.     

Further evidence of involvement of central and peripheral sensory pathways in olivopontocerebellar atrophy

We report the electrophysiological findings of the central and peripheral somatosensory pathways in 20 patients with olivopontocerebellar atrophy. Changes in sensory action potentials of the median nerve were observed in 14 patients and consisted of reduced sensory potential amplitudes associated in 10 cases with an increase in distal latencies. Sixteen out of 20 patients also showed changes in somatosensory evoked potentials after stimulation of the median nerve, consisting of decreased amplitude of N13 (13 cases) and N20 (16 cases) components, associated with increased N9-N13 interpeak latency in 9 and N13-N20 in 14 patients. The origin of these alterations is discussed.     

A study of peripheral cervical and cortical evoked potentials and afferent conduction times in the somatosensory pathway

Somatosensory evoked potentials were recorded from Erb's point (N9), the cervical spine (N14) and the scalp (N20) in 47 volunteer patients to establish the normal impulse conduction time between these recording sites. Either the ulnar or the median nerve or both were stimulated percutaneously, and pure sensory as well as mixed sensorimotor nerve fibres were used. No significant differences in either the N9-N14 or N14-N20 conduction times were found for different sets of peripheral stimuli. The N9-N14 conduction time evidently reflects impulse propagation in the proximal part of the brachial plexus, the cervical roots and the dorsal column. Cross-correlation analysis, however, suggested that the main contribution to this conduction time is a central one, probably the dorsal column. The N14-N20 conduction time represents a pure central conduction time probably between the dorsal column nuclei and the cortex. While the amplitudes, morphologies and latencies of the somatosensory evoked responses N9, N14 and N20 varied significantly, the N9-N14 and N14-N20 conduction times were fairly constant. The results indicate that diagnostic use of the somatosensory evoked potentials based exclusively on the response latencies can be very misleading, both when latencies are normal and when pathologically delayed. In such cases the N9-N14 and N14-N20 conduction times can be conclusive, and we suggest that these times should be included in all SEP tests.     

Somatosensory evoked potentials in Huntington's disease

Scalp recorded somatosensory evoked potentials (SEPs) elicited by left and right median nerve stimulation were obtained in 21 patients with Huntington's disease (HD), 14 individuals at risk (AR) for HD, and 21 non-patient controls matched for age and sex. Although SEP abnormalities were not uniform in the HD group, no HD patient had SEPs that conformed fully to the normal configuration with respect to peak latencies, presence of all components and spatial distribution. The most common abnormality was non-specific in nature, consisting of amplitude reduction or virtual abscence of components after 100 msec. More specific deviations were noted in the early SEP events. In half of the HD patients, peak P30 seemed to occur at approximately 45 msec poststimulus; this peak could have been taken as the normal P45 had it not reversed in phase between the central and frontal leads. In these cases peak P45 prepared to be missing. Peak N20 latency values were longer in the HD group than in the non-patient controls, whereas the P15 latencies did not differ significantly. The conduction time between P15 and N20 was significantly longer in HD patients than the non-patient controls. SEPs of the majority of the ARs were similar to those of the non-patients controls in terms of overall configuration, although mean amplitudes were generally lower for ARs than non-patient controls and 4 ARs exhibited prolonged P15-N20 latency differences.     

Evoked potential studies in mitochondrial encephalomyopathy

Evoked potentials were studied in a patient with a mitochondrial encephalomyopathy revealing a defect of nicotinamideadenine dinucleotide dehydrogenase and cytochrome C oxidase in the mitochondria of a muscle biopsy specimen. The biopsy specimen showed myopathic changes with ragged-red fibers and markedly decreased cytochrome C oxidase in the muscle fibers. Subcortical somatosensory evoked potentials to median nerve stimulation were normal in the peak latencies of N9, N11, and N13. Cortical somatosensory evoked potentials to median nerve stimulation revealed significantly delayed peak latencies of N20, P20, P25, and N26, although N16 latency was normal. In particular, the interpeak latency between N16 and N20 was significantly delayed. In topographic maps, N20 and P20 were delayed in the peak latencies with normal scalp distributions. Dysfunction of somatosensory cortex indicated by the delay of cortical somatosensory evoked potentials may be related to a cortical mitochondrial abnormality. The absence of responses to auditory stimulation within 10 milliseconds could be related to the dysfunction of peripheral acoustic nerves.     

The effect of the selective activation of different peripheral nerve fiber groups on the somatosensory evoked potentials in the cat

Contralateral and ipsilateral cortical somatosensory evoked potentials to selective activation of different diameter sural nerve fiber groups were recorded in cats. Activation of alpha fibers evoked a well defined positive-negative primary potential at the contralateral somatosensory area II. Activation of delta fibers in addition to alpha fibers resulted in another positive-negative wave of comparable amplitude with a latency approximately twice that of the early component. Isolation of the peripheral input to the delta fibers alone, by blocking the alpha fiber activity with the use of triangular pulses, caused the complete disappearance of the initial wave, leaving the second with no latency or amplitude changes. This demonstrated that the latter potential was evoked by delta fibers. Ipsilateral responses followed the same pattern, however with higher peripheral thresholds, longer latencies and smaller amplitudes. No cortical potentials could be recorded to activation of C fibers. The results of this study are at variance with previous observations about the cortical responses to small myelinated nerve fiber activity. The rationale of the use of triangular pulses for selectively activating nerve fiber groups is also discussed.     

Origins of cat somatosensory far-field and early near-field evoked potentials

A complex pattern of potentials evoked by forelimb cutaneous nerve stimulation was recorded from the skull surface of barbiturate anesthetized cats and was resolved by computer averaging. Seven far-field components (designated I-VII) and several larger early near-field components (designated P1, N1, P2, N2 and P3) have been identified from averaged potentials. All far- and early near-field components were elicited by activation of myelinated nerve fibers. Their latency and amplitude depended entirely on the number of large myelinated nerve fibers recruited into the nerve volley. Spinal lesions showed that peripherally evoked far- and early near-field potentials were generated from both lemniscal and extralemniscal sources. Far-field and early near-field potentials were evoked either from the lemniscal system by dorsal column stimulation or from the extralemniscal system by cutaneous nerve stimulation after dorsal column lesions. These potentials were similar in configuration to those evoked by cutaneous nerve stimulation in the intact cat. Sequential rostral to caudal ablations and lesions within the lemniscal or extralemniscal system eliminated the potentials selectively. The following sites of origin were proposed: I--peripheral nerve; II (IIa)--dorsal columns; IIb--spinothalamic tract; III--dorsal column nuclei or medial lemniscus; III, IV--spinocerebellar and spinoreticular tracts; V--lateral reticular nucleus or reticulocerebellar tract; VI, VII--cerebellum; P1--lateral and medial thalamic nuclei or thalamocortical projections; N1, P2--sensorimotor cortical areas; N2, P3--association cortical areas. Lemniscal and extralemniscal far- and early near-field potentials were generated from common as well as separate sites. The latencies of somatosensory far- and early near-field potentials recorded extracranially in this study closely correlated with the latencies of local potentials recorded by others at the proposed lemniscal and extralemniscal sites of origin. The contribution of extralemniscal sources to far- and early near-field potentials and their importance to clinical measurement of somatosensory evoked potentials and diagnosis of neurological disorders are discussed.     

Antiepileptic drug effects on somatosensory evoked potentials

Some evoked potential changes have been documented in chronic phenytoin (PHT), valproate (VPA), or benzodiazepine therapy, whereas other studies have suggested little change with carbamazepine (CBZ) or phenobarbital (PB). We recorded median and posterior tibial nerve somatosensory evoked potentials (SEPs) in complex partial seizure patients taking PHT, CBZ, or VPA in monotherapy with stable therapeutic serum levels and no toxic symptoms. Ten patients each were studied with PHT, CBZ, and VPA and were compared with age-matched controls. Median nerve responses were recorded at Erb's point, cervical spine, and contralateral cerebral sites; tibial nerve evoked potentials were recorded from popliteal fossa, lumbar, cervical spine, and midline scalp electrodes. Epileptic patients and controls did not differ in SEP latency, amplitude, or central condition time. PHT prolonged Erb's point and popliteal fossa latencies, but not central conduction time. CBZ had no effect on latencies or amplitudes. Evoked potential amplitudes were reduced by VPA, and cortical response latencies were minimally prolonged. Chronic antiepileptic therapy without toxicity had little effect on SEPs. PHT may have a slight effect on peripheral nerve conduction, and VPA may have an effect on amplitude of cerebral responses.     

Spinal roots of rats poisoned with methylmercury: physiology and pathology

The evoked potentials in the ventral and dorsal roots were recorded independently by stimulating the sciatic nerve of both control and methylmercury-poisoned rats. Poisoned rats showed markedly decreased amplitudes but normal latencies of the potentials evoked in the dorsal roots. Potentials evoked in the ventral roots had normal latencies and amplitudes. Pathological correlates indicated acute axonal degeneration of the dorsal roots, with a significant decrease of the large and small myelinated fiber densities. The ventral roots were histologically unremarkable. Our pathological confirmation of the electrophysiologic changes in the methylmercury-poisoned rats enables us to substantially assess the pathophysiological aspects of acute lesions in the spinal roots.     

Evoked potentials in olivopontocerebellar atrophy

Pattern-reveral visual evoked potentials, far-field and cortical somatosensory evoked potentials, and auditory brainstem potentials were recorded in two patients with olivopontocerebellar atrophy. In one patient, visual evoked potentials exhibited prolonged latency and interocular latency differences in the absence of clinical visual dysfunction. Median and tibial nerve evoked cortical potentials were severely attenuated in the absence of somatosensory deficit or peripheral nerve slowing. The far-field somatosensory potentials, however, were well preserved. All components of the auditory brain-stem potentials had latencies within normal limits. In the other, more severely afflicted, patient, all visual, somatosensory, and auditory evoked potentials were abnormal.     

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.     

Stage II sleep alters infants' short latency somatosensory evoked potentials

To evaluate the effects of stage II sleep on short latency somatosensory evoked potentials (SLSEP) to median nerve stimulation, we studied 16 normal infants from two to twelve months of age. SLSEP were recorded during waking and stage II sleep. Four channels of parasagittal EEG and behavioral observations were used to classify states. Compared with SEP in the waking state, cerebral potentials in stage II sleep were of much lower amplitude, even vanishing entirely in several infants. In addition, the change from waking to stage II sleep produced significantly longer latencies of the peaks N1, P1, and P2. We suggest performing SLSEP in infants in the waking state in order to assess cerebral somatosensory function.     

Effects of age on event-related potentials in chronic alcoholics: a multimodal study.

To test different versions of the premature aging hypothesis in alcoholics, brainstem auditory evoked potentials (BAEPs), long-latency auditory evoked potentials (LAEPs), P3 and visual evoked potentials (VEPs) were recorded in 32 alcoholic subjects. The phenomena in patients' event-related potentials (ERPs) differ from those observed in normal aging subjects and become more pronounced with age. ANOVA showed a significant effect by group (alcoholic patients/controls) on certain parameters of BAEPs (III, III-V, I-V), VEPs (P100 latency) and LAEPs (N1-P2 amplitude and N2 latency) unaffected by age, while age had a significant effect on some parameters of LAEPs (N2-P3 amplitude, P3 latency) unaffected, or less affected by chronic alcohol consumption. At a clinical level, abnormalities in BAEPs and VEPs seem good early trouble indices in alcoholic patients, while alterations in latencies and amplitudes of LAEPs appear in older patients. These data seem to be in favor of a critical age or critical abuse in the action of alcohol, in place of the classical hypothesis of premature aging.     

Peroneal somatosensory evoked potentials in the "pure" form of hereditary spastic paraplegia

Two patients suffering from the stationary form of hereditary spastic paraplegia, father and son, are described. While in the father the disease - probably because of congenital clubfeet - led to flexion contractures of the hip- and knee-joints, the son in contrary showed extreme genua recurvata. In spite of these contradictionary findings, neurological examination of both patients led to the diagnosis of stationary form of hereditary spastic paraplegia. Both patients had normal latencies of their somatosensory evoked peroneal cortical potentials (Peron-SEP). It is known that the progredient form of the disease leads to alterations of the Peron-SEP. So it is the opinion of the authors that this electrodiagnostic aspect might allow to distinguish between the "pure" and the progredient form of the disease in less clear cases, if these findings can be confirmed in other sibships with the "pure" form of hereditary spastic paraplegia.