Cerebral evoked potentials after stimulation of the posterior urethra in man

Cerebral evoked potentials (EPs) were recorded in 25 neurologically normal subjects aged 22–73 years (mean 44.0) after stimulation of the posterior urethra (PU) and the pudendal nerve. After maximal PU stimulation 2 different configurations of the potential were found. In 12 cases a simple bi-triphasic wave form was recorded while in 12 cases there was a bifid form of the first negative wave. In 1 case identical EPs were recorded after PU and pudendal nerve stimulation.It was concluded that (1) PU stimulation excites fibres in the pudendal nerve at higher stimulation strength, resulting in a bifid wave form of the cerebral evoked potential in some individuals, (2) the most prominent negative peak, N1, with a latency of 102.1 ± 13.2 msec, is the most reproducible part of the PU-evoked potential, (3) the N1 is probably transmitted through Aδ fibres localized in the pelvic nerves, (4) there are differences between individuals concerning pudendal and pelvic nerve involvement in afferent innervation of the urethra.     

Topography of middle-latency somatosensory evoked potentials following painful laser stimuli and non-painful electrical stimuli

The aim of this study was to compare cerebral evoked potentials following selective activation of Aβ and Aδ fibers. In 15 healthy subjects, Aβ fibers were activated by electrical stimulation of the left radial nerve at the wrist. Aδ fibers were activated by short painful radian heat pulses, applied to the dorsum of the left hand by a CO₂ laser. Evoked potentials were recorded with 15–27 scalp electrodes, evenly distributed over both hemispheres (bandpass 0.5–200 Hz). The laser-evoked potentials exhibited a component with a mean peak latency of 176 msec (N170). Its scalp topography showed a parieto-temporal maximum contralateral to the stimulus side. In contrast, the subsequent vertex negativity (N240), which appeared about 60 msec later, had a symmetrical scalp distribution. Electrically evoked potentials showed a component at 110 msec (N110), that had a topography similar to the laser-evoked N170. The topographies of the N170 and N110 suggest that they may both be generated in the secondary somatosensory cortex. There was no component in the electrically evoked potential that had a comparable interpeak latency to the following vertex potential: for N60 it was longer, for N110 it was shorter. On the other hand, in the laser-evoked potentials no component could be identified the topography of which corresponded to the primary cortical component N20 following electrical stimulation.     

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.     

Selectivity of attenuation (i.e., gating) of somatosensory potentials during voluntary movement in humans

Attenuation of somatosensory evoked potentials (SEPS) recorded from the scalp during voluntary movement occurs for specific combinations of the finger moved and the peripheral nerve stimulated. The cerebral potential component occurring at a latency of 27 msec (P27) evoked either by stimulation of median nerve at the wrist or by stimulation of 1st and 2nd digit nerves in the fingers were selectively attenuated during movement of 1st digit but were not altered during movement of 5th digit. By contrast, the cerebral P27 component evoked by stimulation of ulnar nerve at the wrist or by stimulation of 5th digital nerve were attenuated during movement of that digit but were not altered during movement of 1st digit. Gating of somatosensory activity is a selective phenomenon occuring when movement involves the areas being stimulated.     

Neurophysiological evaluation of central-peripheral sensory and motor pudendal fibres

Extensive neurophysiological investigations were carried out in 18 healthy volunteer subjects, and 6 patients with neurological disease. The tests consisted of spinal and scalp somatosensory evoked potentials (SEPs) to stimulation of the dorsal nerve of penis/clitoris, motor evoked potentials (MEPs) from the bulbocavernosus muscle (BC) and anal sphincter (AS) in response to scalp and sacral root stimulation, and measurement of sacral reflex latency (SRL) from BC and AS.In the control subjects, the mean sensory total conduction time (sensory TCT), as measured at the peak of the scalp P40 wave was 40.9 msec (range: 37.8–44.2). The mean sensory central conduction time (sensory CCT = spine-to-scalp conduction time) was 27.0 msec (range: 23.5–30.4).Transcranial brain stimulation was performed by using a magnetic stimulator both at rest and during voluntary contraction of the examined muscle. Sacral root stimulation was performed at rest. Motor total conduction times (motor TCT) to BC and AS muscles were respectively 28.8 and 30.0 msec at rest, and 22.5 and 22.8 msec during contraction. Motor central conduction times (motor CCT) to sacral cord segments controlling BC and AS muscles were respectively 22.4 and 21.2 msec at rest, and 15.1 and 12.4 msec during contraction.The mean latencies of SRL were respectively 31.4 msec in the bulbocavernosus muscle and 35.9 msec in the anal sphincter. Combined or isolated abnormalities of SEPs, MEPs and SRL were found in a small group of patients with neurological disorders primarily or secondarily affecting the genito-urinary tract.     

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.     

Spontaneous Activity in Crustacean Neurons

Single units which discharged with regular spontaneous rhythms without intentional stimulation were observed in the ventral nerve cord by intracellular recording close to the sixth abdominal ganglion. These units were divided into two groups: group A units in which interspike intervals varied less than 10 msec.; group B units in which interspike intervals varied within a range of 10 to 30 msec. Group A units maintained "constant" interspike intervals and could not be discharged by sensory inputs, while the majority of group B units could be discharged by appropriate sensory nerve stimulation. Both group A and B units discharged to direct stimulation when the stimulating and recording electrodes were placed in the same ganglionic intersegment, and directly evoked single spikes reset the spontaneous rhythm. In group B units, presynaptic volleys reset the spontaneous rhythm of some units; but in others, synaptically evoked spikes were interpolated within the spontaneous rhythm without resetting. The phenomenon of enhancement could also be demonstrated in spontaneously active units as a result of repetitive stimulation. It is concluded that endogenous pacemaker activity is responsible for much of the regular spontaneous firing observed in crayfish central neurons, and that interaction of evoked responses with such pacemaker sites can produce a variety of effects dependent upon the anatomical relationships between pacemaker and synaptic regions.     

Pudendal nerve somatosensory evoked potentials in paediatrics: maturation aspects

Pudendal nerve somatosensory evoked potentials (PN-SSEPs) were recorded in 21 healthy children (age range: 3.3–13.3 years). The dorsal nerve of the penis/clitoris was stimulated and SSEPs were recorded at spinal L1-D12 and at cortical Cz′-Fz. Morphology, latency and amplitude of the cortical SSEPs were evaluated. A cortical response was obtained in all but two subjects. Cortical SSEPs were broader and less defined in shape in the youngest subjects. There was a progressive shortening of the latency of the P and N components during growth. Spinal responses were obtained only in 6 cases. Nine subjects also underwent tibial nerve stimulation. Pudendal and tibial SSEPs differed in their degree of maturation.     

Short and middle latency vestibular evoked responses to acceleration in man

We have succeeded in recording short and middle latency vestibular evoked responses in human subjects. The head was held rigidly in a special, patented head holder, constructed individually for each subject, which gripped the teeth of the upper jaw. The stimulus consisted of 2/sec steps of angular acceleration impulses produced by a special motor with intensities of about 10,000°/sec² and with a rise time of 1–2 msec. The electrical activity was recorded as the potential difference between special forehead and mastoid electrodes having a large, secure contact area with the skin. The activity was digitally filtered and averaged in 2 separate channels by means of a Microshev 2000 evoked response system. The short latency responses, with peaks at about 3.5 msec (forehead positive), 6.0 msec (forehead negative) and 8.4 msec (forehead positive; bandpass: 200–2000 Hz; average of 1024 trials), had amplitudes of about 0.5 μV. The middle latency responses had peaks at about 8.8 msec (forehead positive), 18.8 msec (forehead negative) and 26.8 msec (forehead positive; 30–300 Hz; N = 128 trials), with larger amplitudes (about 15 μV). These responses were consistently recorded in the same subject at different times and were similar in different normal subjects. Strenuous control experiments were conducted in order to ensure that these responses are not artefacts due to the movement of conducting media (head, electrodes and leads) in the electromagnetic field of the motor and are elicited by activation of normal labyrinths. Among other controls, they were not present in a cadaver, in patients with bilateral absence of nystagmus to caloric stimuli and in conducting volumes the size of the human head. They were also not masked by white noise.     

Cerebral responses evoked by stimulation of the vesico-urethral junction in normal subjects

Following the bipolar stimulation of the vesico-urethral junction (VUJ), evoked potentials (EPs) with a late and prominent negativity (mean latency 91.4 ± 11.0 msec) were recorded from scalp in 22 male subjects. Although remarkable intersubject variations occurred, no peak variation could be seen in any given subject. Maximum amplitude of the EPs was recorded from Cz and CzP points. Stimuli with various frequencies did not lead to any differences in shape and latency of EPs.The differences between the EPs by bipolar stimulation of the VUJ and the responses elicited by distal urethal and pudendal nerve stimulation suggest that, during bipolar stimulation of VUJ, the somatic afferents were not excited. Therefore, these responses were most likely due to the excitement of the visceral afferents arising from the VUJ separately. This method may be a useful technique for evaluating the physiological condition of the afferent nerves arising from VUJ.     

Vestibular projections in the cat temporal cortex

Boundaries of vestibular projections in the temporal cortex during stimulation of the vestibular nerve were studied in cats anesthetized with pentobarbital and chloralose or chloralose alone. The caudal boundary of the vestibular zone was shown to run along the anterior ectosylvian gyrus. A focus of evoked activity was found in the suprasylvian sulcus or 1–2 mm rostrally to it. All short-latency evoked potentials recorded during vestibular nerve stimulation in the temporal region caudally to the zone mentioned above were connected with the spread of current to auditory structures. To verify the extent of spread of the stimulating current, focal potentials were recorded in the vestibular and superior olivary groups of nuclei. Special experiments were carried out to study the topography of these potentials at the level of bulbar structures during stimulation of vestibular and auditory nerves. According to the results, there is no second vestibular area in the temporal cortex in cats. Vestibular afferentation is projected mainly into the contralateral hemisphere, and the response latency is 5.2±0.7 msec. The ipsilateral evoked potentials had a long latent period (8.4±1.3 msec), and their amplitude depended on the type of anesthesia; it was accordingly postulated that additional synaptic relays exist in this vestibulocortical pathway.     

A method of calculating spinal cord transit time from potentials evoked by tibial nerve stimulation in normal subjects and in patients with spinal cord disease

Somatosensory potentials were evoked by stimulation of the tibial nerve at the ankle and recorded over the spine and scalp in 16 normal subjects and 26 patients with known or suspected spinal cord disease, with the aim of developing a method of measuring spinal sensory conduction velocity using a tolerable number of stimuli, applied unilaterally to alert subjects.In normal subjects N21 was consistently recorded overL1 vertebra and in most subjects a complex, N27/N29/P33, was recorded over the cervical spine referred to the vertex. Constant latencies at different spinal levels and, in one subject, comparison with the latency of the ascending volley indicate that the complex was not derived from the spinal cord but from more rostral structures, and therefore only transit time, rather than velocity, could be measured.In patients with clinically definite multiple sclerrosis, even with minimal clinical signs, the N27/N29/P33 complex was always abnormal. Abnormalities in this and other forms of spinal cord disease were commonly absence or distortion of the complex, prolonged transit time being rare. The clinical value of the method is limited by the very low amplitude of the responses.     

Pain-related somatosensory evoked potentials following CO2 laser stimulation of foot in man

Since our previous study of pain somatosensory evoked potentials (SEPs) following CO₂ laser stimulation of the hand dorsum could not clarify whether the early cortical component NI was generated from the primary somatosensory cortex (SI) or the secondary somatosensory cortex (SII) or both, the scalp topography of SEPs following CO₂ laser stimulation of the foot dorsum was studied in 10 normal subjects and was compared with that of the hand pain SEPs and the conventional SEPs following electrical stimulation of the posterior tibial nerve recorded in 8 and 6 of the 10 subjects, respectively. Three components (N1, N2 and P2) were recorded for both foot and hand pain SEPs. N1 of the foot pain SEPs was maximal at the midline electrodes (Cz or CPz) in all data where that potential was recognized, but the potential field distribution was variable among subjects and even between two sides within the same subject. N1 of the hand pain SEPs was maximal at the contralateral central or midtemporal electrode. The scalp distribution of N2 and P2, however, was not different between the foot and hand pain SEPs. The mean peak latency of N1 following stimulation of foot and hand was found to be 191 msec and 150 msec, respectively, but there was no significant difference in the interpeak latency of Nl-N2 between foot and hand stimulation. It is therefore concluded that NI of the foot pain SEPs is generated mainly from the foot area of SI. The variable scalp distribution of the N7 component of the foot pain SEPs is likely due to an anatomical variability among subjects and even between sides.     

Spine and scalp somatosensory evoked potentials in normal subjects and patients with spinal cord disease: Evaluation of afferent transmission

Spine and scalp somatosensory evoked potentials (SEPs) to peroneal nerve stimulation were recorded from 20 normal subjects using 1 restricted and 3 open frequency filter bandpasses. Spine to spine and spine to scalp propagation velocities were calculated. Of those recording parameters investigated, optimal recordings were obtained using an open bandpass (5–1500 or 30–1500 Hz) and recording from 3 surface spine bipolar channels and 1 scalp bipolar channel. This method was then investigated in 40 patients with disease of the spinal cord and peripheral nervous system. Focal spinal cord compressive lesions generally resulted in slowing of spine to spine and spine to scalp propagation velocities. Diffuse or multifocal lesions of the spinal cord generally resulted in the absence of scalp responses. Although there was no consistent correlation of the SEP findings with the sensory exam, there was a correlation of the SEP findings with the clinical prognosis.     

Cerebral evoked potentials after rectal stimulation

We obtained reproducible cortical evoked potentials (EPs) in response to electrical stimulation of the rectum with 1 Hz frequency. We found 2 distinctly different EPs in response to rectal stimulation. In 5 females, the EP had an early onset latency (mean 26 msec) with multiple positive and negative peaks. In 10 females, the EP had a later onset latency (mean 52 msec) and a trifid configuration, having a very prominent negative peak. The early onset EPs after rectal stimulation appeared very similar to the wave form of the cortical EPs recorded after pudendal nerve stimulation. Finding similar interpeak latencies in the early onset EP after rectal stimulation and the EP after pudendal nerve stimulation suggests that either the same pathway was used or that rectal stimulation also stimulated the pudendal nerve. It appears that we stimulated visceral afferents when we recorded late onset EPs, because the large EP amplitude declined rapidly with faster stimulation rates and also with greater number of averaging, and the sensation threshold was very unstable, all different to somatosensory EPs.     

Early scalp responses evoked by stimulation of the supraorbital nerve in man

In 25 healthy volunteers the supraorbital nerve was stimulated and evoked potentials were recorded. Leads were placed on the scalp and along the ipsilateral eyebrow-mastoid line and were either referred to a non-cephalic reference (on the neck, or Cv7) or linked to form bipolar derivations. As template wave form was chosen the one obtained from derivation Cz-Cv7, which had an initial triphasic component with negative (SW1a), positive (SW1b), negative (SW1c) polarity (mean latencies 0.63, 0.95 and 1.43 msec), followed by 2 negative waves (SW2 and SW3, mean latencies of 2.20 and 2.89 msec). A final positive wave could be observed in most cases (SP4, mean latency of 4.08 msec). The records collected from the various derivations showed that each component (SW1, SW2, SW3 and SP4) had a different behaviour, thus suggesting separate origins. SW1 would originate from a volley travelling from the point of stimulation towards the mastoid, probably across the ophthalmic branch of the trigeminal nerve. The subsequent components would be generated by deeply situated structures: double pulse stimulation suggests that SW1, SW2 and SW3 are generated before the first synapse, whereas SP4 is a postsynaptic event. A strong similarity exists between the components evoked by stimulation of the supraorbital and the infraorbital nerves. Local anaesthetic block of the frontal nerve on the stimulated side and monitoring of the EMG activity of m. orbicularis oculi and m. frontalis ruled out any muscle contamination of the responses described in this paper.     

Functional characteristics of the input-output correlation in the frog vestibular nuclei

Field and intracellular potentials were recorded in the vestibular nuclear complex of the frog perfused brain following stimulation of the anterior branch of the ipsilateral vestibular nerve and spinal cord. Mono- and polysynaptic EPSPs with orthodromic APs were recorded from vestibular neurones following vestibular nerve stimulation. Antidromic activation of neurones sending their axons to the labyrinth was also recorded. Antidromic APs of vestibulo-spinal neurones evoked with mean latency of 1.43 and 2.19 ms to stimulation of cervical and lumbar cords, respectively, were revealed.     

Direct recording of somatosensory evoked potentials in the vicinity of the dorsal column nuclei in man: their generator mechanisms and contribution to the scalp far-field potentials

Somatosensory evoked potentials (SEPs) in the vicinity of the dorsal column nuclei in response to electrical stimulation of the median nerve (MN) and posterior tibial nerve (PTN) were studied by analyzing the wave forms, topographical distribution, effects of higher rates of stimulation and correlation with components of the scalp-recorded SEPs. Recordings were done on 4 patients with spasmodic torticollis during neurosurgical operations for microvascular decompression of the eleventh nerve. The dorsal column SEPs to MN stimulation (MN-SEPs) were characterized by a major negative wave (N1; 13 msec in mean latency), preceded by a small positivity (P1) and followed by a large positive wave (P2). Similar wave forms (P1′-N1′-P2′) were obtained with stimulation of PTN (PTN-SEPs), with a mean latency of N1′ being 28 msec. Maximal potentials of MN-SEPs and PTN-SEPs were located in the vicinity of the ipsilateral cuneate and gracile nuclei, respectively, at a level slightly caudal to the nuclei. The latencies of P1 and N1 increased progressively at more rostral cervical cord segments and medulla, but that of P2 did not. A higher rate of stimulation (16 Hz) caused no effects on P1 and N1, while it markedly attenuated the P2 component. These findings suggest that P1 and N1 of MN-SEPs, as well as P1′ and N1′ of PTN-SEPs, are generated by the dorsal column fibers, and P2 and P2′ are possibly of postsynaptic origin in the respective dorsal column nuclei.The peak latency of N1 recorded on the cuneate nucleus was identical with the scalp-recorded far-field potential of P13–14 in all patients, while no scalp components were found which corresponded to P2. These findings support the previous assumption that the scalp-recorded P13–14 is generated by the presynaptic activities of the dorsal column fibers at their terminals in the cuneate nucleus.     

Botzinger complex region role in phrenic-to-phrenic inhibitory reflex of cat

Neuronal recordings, microstimulation, and electrolytic and chemical lesions were used to examine the involvement of the B?tzinger Complex (B?tC) in the bilateral phrenic-to-phrenic inhibitory reflex. Experiments were conducted in decerebrate cats that were paralyzed, ventilated, thoracotomized, and vagotomized. Microelectrode recordings within the B?tC region revealed that some neurons were activated by phrenic nerve stimulation (15 of 69 expiratory units, 9 of 67 inspiratory units, and 19 nonrespiratory-modulated units) at average latencies similar to the onset latency of the phrenic-to-phrenic inhibition. In addition, microstimulation within the B?tC caused a short latency transient inhibition of phrenic motor activity. In 17 cats phrenic neurogram responses to threshold and supramaximal (15 mA) stimulation of phrenic nerve afferents were recorded before and after electrolytic B?tC lesions. In 15 animals the inhibitory reflex was attenuated by bilateral lesions. Because lesion of either B?tC neurons or axons of passage could account for this attenuation, in eight experiments the phrenic-to-phrenic inhibitory responses were recorded before and after bilateral injections of 5 microM kainic acid (30-150 nl) into the B?tC. After chemical lesions, the inhibitory response to phrenic nerve stimulation remained; however, neuronal activity typical of the B?tC could not be located. These results suggest that axons important in producing the phrenic-to-phrenic reflex pass through the region of the B?tC, but that B?tC neurons themselves are not necessary for this reflex.     

Membrane lipids of human peripheral nerve and spinal cord.

Major membrane lipids were determined in specimens of human peripheral nerve (cauda equina) and spinal cord of 10 subjects aged 20-70 years. The same lipids were also assayed in myelin from the same tissues isolated with two different procedures and in myelin of cauda equina from 3 subjects aged 17-91 years isolated with a third method. The concentrations (mean and standard deviation) of phospholipids were 90 +/- 11 and 96 +/- 9 nmol/g fresh weight; of cholesterol 70 +/- 15 and 101 +/- 16; of cerebroside 19 +/- 3 and 41 +/- 7; of sulfatide 10 +/- 1 and 11 +/- l; and of gangliosides 0.80 +/- 0.08 and 0.40 +/- 0.05 N in cauda equina and spinal cord, respectively. The proportion of ethanolamine phosphoglyceride was lower and that of sphingomyelin higher in cauda equina than in spinal cord. The myelin of peripheral nerve and spinal cord contained almost the same proportions of lipids as the whole tissue. The protein-bound sialic acid content was 3-fold higher than the lipid-bound sialic acid content in cauda myelin. The fatty acid patterns of choline, ethanolamine, inositol and serine phosphoglycerides of spinal cord and its myelin, were very similar to those of cerebral white matter, while the phosphoglycerides of cauda equina had higher proportions of monoenoic acids and lower proportions of polyunsaturated fatty acids. The fatty acid patterns of sphingomyelin, cerebroside and sulfatide of spinal cord were similar to those of cerebral white matter, while those of cauda equina contained significantly more saturated fatty acids. This suggests that the lipid and fatty acid compositions of peripheral nerve are particularly suitable for the formation of a tightly packed myelin membrane which can be a powerful shield against infections and other injuries.