Recovery of neuronal transmission after prolonged cerebral ischemia

The potentials of postischemic functional recovery were studied in cats submitted to 1 h of complete cerebrocirculatory arrest in normothermia. Neuronal activity was estimated by recording the electroencephalogram (EEG), the pyramidal response following stimulation of the motor cortex and the somatosensorily evoked cortical potentials. During ischemia EEG was suppressed within 12-15 s, evoked potentials within 2 min, and the pyramidal response within 5 min. After recirculation following ischemia, the electrically evoked D wave of the pyramidal response began to reappear between 7 and 9 min and the synaptically evoked I wave between 25 and 60 min. The evoked cortical potentials returned in parallel with the I wave of the pyramidal response but control amplitude was not reached before 3 h. The peak latencies of the evoked potentials were consistently prolonged for at least 24 h but normalized after a few days, provided secondary postischemic circulatory disturbances could be prevented. EEG began to recover after the beginning appearance of the somatosensorily evoked cortical potentials; initially it exhibited a burst-suppression pattern but it gradually progressed to continuous activity. The frequency pattern of the EEG normalized within 24 h and the amplitude after a few days. After recovery, the behavior of the pyramidal response and of evoked potentials to repetitive stimulation was the same as under control conditions.     

The median nerve evoked potential in normal children and youths: normal values]

The derivation of cortical somatosensory evoked potentials permits a good local and functional diagnosis of supratentorial structures and the localisation of damage in this area. The special diagnostical relevance of early cortical somatosensory evoked potentials as a sage, non-invasive examination method in pediatric neurology is given both by these characteristics and by the fact that they cannot, in principle, be influenced by sleep or by drugs affecting the central nervous system. Somatosensory evoked cortical potentials of N. medianus were investigated for 35 children (17 boys, 18 girls) between the ages of 6 and 17, for whom there were no anamnestic or clinical indications of neurological or otological diseases. Investigations demonstrate that the SEPs of the N. medianus from the P15 up to and including the N55, is in every case clearly measurable in children from preschool age up to the end of adolescence. In the evaluation of the cortical SEPs, the P15, N20 and P25 were considered to be the components most stable and those most valuable for clinical practice. These could also be presented with the smallest standard deviations and side differences. The latencies of the P15 and N20 of the N. medianus show significant dependencies on the height of the children. The later potential components, side differences, interpeak intervals and amplitudes show no correlations with height. The SEPs of N. medianus show no dependencies on gender or on physical parameters such as weight or head circumference of the experiments. In summary it can be established that, using the procedure mentioned above, the cortical somatosensory evoked potentials in children can be described well and reproducibly and within practical narrow standard limits.     

Cerebral potentials evoked by electrical stimulation of the anal canal

We describe the procedure with which cortical potential responses are evoked by a stimulation of the anal canal to assess the integrity of its sensory pathways. These potentials were recorded in 66 patients. In 44 patients, a cortical evoked response was obtained with a succession of positive and negative peaks, W shaped (35 cases) or V shaped (nine cases). In seven cases, cortical responses were interpreted differently by two independent observers. In these seven patients, such differences could be explained by an insufficient amplification of the recorded electrical waves recorded on paper (<10 mm). Fifteen patients gave no cortical response. Eight had a neurologic disease that could explain the lack of response. In the seven others, the absence of response was considered as false negative, but six of these stimulations had been carried out during the first part of the study. There is some evidence that cortical evoked potentials may be obtained after an electrical stimulation of the anal canal, but a training period seems necessary to master the technique and obtain reproducible and recognizable responses.Supported by a grant from the INSERM, 101 rue de Tolbiac 75654 Paris Cedex 13.     

The effect of temperature, mean arterial pressure, and cardiopulmonary bypass flows on somatosensory evoked potential latency in man

Median nerve somatosensory evoked potentials were recorded in 21 patients undergoing cardiac surgical procedures utilizing cardiopulmonary bypass, in order to establish the effects of hypothermia, reductions in mean arterial pressure, and alterations in cardiopulmonary bypass flows on evoked potential latency. Induction and maintenance of anesthesia with fentanyl caused a significant prolongation of latency of the first cortical peak. Temperature changes were linearly correlated with changes in latency for peaks recorded from Erb's point (r = -0.843, p less than 0.01) and the contralateral cortex (r = 0.843, p less than 0.01). There was no significant effect of mean arterial pressure or cardiopulmonary bypass flow reductions on latencies under the conditions of this study. Our results emphasize the importance of monitoring peripheral and first cortical peak latencies in evaluating somatosensory evoked potentials. It is suggested that peak latency prolongations beyond those predicted by temperature alterations may be indicative of hypoperfusion.     

Peripheral,synaptic and central neuronal transmission is affected in type 1 diabetes

AimsWe hypothesized that adults with type 1 diabetes and severe polyneuropathy have alterations in neuronal transmission at different anatomical levels. The aims were to investigate upstream sensory neuronal activation in terms of peripheral, spinal, precortical, and cortical transmission.Methods48 participants with type-1 diabetes and polyneuropathy, and 21 age-matched healthy participants were included. Electrophysiological median nerve recordings were used to analyze peripheral transmission at Erb's point (P9-N11); spinal evoked potentials at Cv7 (P11-N14); subcortical evoked potentials at Oz (N14-P18); early cortical evoked potentials at CP5 (N20-P22); late cortical evoked potentials at C1 (N60-P80) and estimated cortical inter-peak latencies as measures of central conduction time.ResultsIn comparison to healthy, the presence of diabetes prolonged peripheral transmission at P9 and N11 (+0.49 ms, p = .000; +0.47 ms, p = .04, respectively), early cortical evoked potentials at CP5: N20 (+2.41 ms, p = .003) and P22 (+5.88 ms, p = .001) and cortical potentials at C1: N60 (+39.08 ms, p = .001) and P80 (+54.55 ms, p = .000) and central conduction time.Decreased amplitudes were shown peripherally (−2.13 μV, p = .000), spinally (−0.57 μV, p = .005) and pre-cortically (−0.22 μV, p = .004).In both healthy and people with diabetes increased central conduction time were associated with decreased parasympathetic tone (ρ = −0.52, p = .027; ρ = −0.35, p = .047, respectively).ConclusionNeuronal afferent transmission and brain responses were significantly impaired in diabetes and the presence of prolonged central conduction time is indicative of severe extensive neuronal damage.Trial registry number: EUDRA CT: 2013-004375-12; clinicaltrials.gov: NCT02138045.     

Generators of somatosensory evoked potentials following leg nerve stimulation

Stimulation of the tibial nerve results in complex spinal potentials evoked from the lumbosacral segments of the spinal cord. These potentials suggest the interaction of different generators. Characteristically a triphasic potential can be recorded from L1. It is composed out of an afferent volley in the dorsal roots (R-response) a synaptically strengthened S-response (N21) and a descending reflexly evoked ventral root discharge (A-wave). Above cervical segments of the spinal cord the evoked potentials are probably composed of the afferent volley in the posterior columns (N24), the activity of the nucleus gracilis (N27) and the volley in the medial lemniscus (P30). The primary cortical response P40 is regarded as the specific activity of the somatosensory foot area.     

Clinical utility of somatosensory evoked potentials in diabetes mellitus

The posterior tibial nerve and median nerve somatosensory evoked potentials (PTN-SEPs and MN-SEPs) were investigated in 34 patients with diabetes mellitus (DM). We measured the latency of the first positive cortical potential (the cortical P37) of PTN-SEPs and that of the first negative cortical potential (the cortical N18) and Erb's potential of MN-SEPs. In 18 patients (52.9%), the cortical P37 latency was more than 3 SD longer than normal in the tibial nerve. There were positive correlations between the latency of cortical P37 and the duration of DM and the motor nerve conduction velocity of the posterior tibial nerve. Sensory action potentials of the posterior tibial nerve were not detectable in 21 patients, though cortical P37 potential was unambiguously recorded by stimulating the posterior tibial nerve even in those subjects. Diabetic retinopathy and nephropathy also tended to rise with increasing latency of cortical P37. The latency of cortical P37 is an important parameter in assessing diabetic neuropathy.     

Age changes in early somatosensory evoked potentials

There are characteristic age-related changes in the cervical and early cortical somatosensory potentials evoked by electrical stimulation of the median nerve. At an age of 40 to 50 years the latencies of the potential components and the transit times start increasing progressively. Moreover, there is an attenuation of the cervical and an enhancement of the cortical components with age. Considering the presumed neuronal basis of the bioelectric phenomena the changes are discussed in connection with aging processes of the spinal ganglion cells, cortical pyramidal cells and the locus coeruleus.     

Real-time imaging of human cortical activity evoked by painful esophageal stimulation

BACKGROUND & AIMS: Current models of visceral pain processing derived from metabolic brain imaging techniques fail to differentiate between exogenous (stimulus-dependent) and endogenous (non-stimulus-specific) neural activity. The aim of this study was to determine the spatiotemporal correlates of exogenous neural activity evoked by painful esophageal stimulation. METHODS: In 16 healthy subjects (8 men; mean age, 30.2 +/- 2.2 years), we recorded magnetoencephalographic responses to 2 runs of 50 painful esophageal electrical stimuli originating from 8 brain subregions. Subsequently, 11 subjects (6 men; mean age, 31.2 +/- 1.8 years) had esophageal cortical evoked potentials recorded on a separate occasion by using similar experimental parameters. RESULTS: Earliest cortical activity (P1) was recorded in parallel in the primary/secondary somatosensory cortex and posterior insula (approximately 85 ms). Significantly later activity was seen in the anterior insula (approximately 103 ms) and cingulate cortex (approximately 106 ms; P=.0001). There was no difference between the P1 latency for magnetoencephalography and cortical evoked potential (P=.16); however, neural activity recorded with cortical evoked potential was longer than with magnetoencephalography (P=.001). No sex differences were seen for psychophysical or neurophysiological measures. CONCLUSIONS: This study shows that exogenous cortical neural activity evoked by experimental esophageal pain is processed simultaneously in somatosensory and posterior insula regions. Activity in the anterior insula and cingulate-brain regions that process the affective aspects of esophageal pain-occurs significantly later than in the somatosensory regions, and no sex differences were observed with this experimental paradigm. Cortical evoked potential reflects the summation of cortical activity from these brain regions and has sufficient temporal resolution to separate exogenous and endogenous neural activity.     

Somatosensory evoked potentials following tactile skin stimulation

Somatosensory evoked potentials were recorded for tactile stimuli applied to the fingers II and V as well as paravertebrally. The advantage of the painless mechanical stimuli is their specificity and the well defined stimulus localization. The question was therefore if the evoked responses are clearly demarcated. Nack potentials (N22: 22.5 and 22.3 ms) as well as cortical SEP's (P1: 33.2 and 32.8 ms) were easily to derive. It was also possible to get SEP's for segmental paravertebral tactile stimuli. For the finger stimulation an Erb's potential could not be recorded reliably.     

Determination of neurophysiological parameters of the aging CNS. I. Evoked potentials (author's transl)]

Somatosensory (SEP) and visual (VEP) evoked potentials were studied in 65 healthy subjects who ranged in age from 62-91 years and in 48 normal persons aged 18-38 years. The amplitudes and latencies of the different components of the evoked potentials were measured. The transmission of evoked potentials from the specific response area into different regions of the ipsi- and contralateral hemisphere were studied. The findings can be summarized as follows: The latencies of the SEP and VEP of aged subjects are significantly prolonged. The increase in latency is relatively slight for the first components, progressively higher for the following components. The amplitudes of the different components of the SEP and VEP are significantly increased in aged subjects. The modifications of the SEP-latencies and of the VEP-amplitudes are more important over the dominant hemisphere. In young subjects the SE are confirmed to the centro-parietal region. In aged persons the SEP spreads over the whole hemisphere. The hypothesis that the aging process involves the synaptic transmitter mechanisms at the cortical level is discussed in relation to the involvement of the latencies. The increase in amplitude of the evoked potentials could be explained by assuming that the inhibition - an essential property of the cortex - decreases during the aging process.     

CENTRAL NERVOUS SYSTEM ACTIVITY ASSOCIATED WITH PAIN EVOKED BY BRADYKININ AND ITS ALTERATION BY MORPHINE AND ASPIRIN

Synthetic bradykinin, a nonapeptide formed from alpha-2 globulin in plasma, injected intra-arterially or intraperitoneally in cats in doses of 10-50 mug, evoked activity in the central nervous system in pathways associated with the signaling of pain. Similar injections of bradykinin in intact normal cats and dogs evoked manifestations of pain, and in conscious humans elicited verbal reports of pain perceived in the area of injection. Single unit activity was recorded in the medial reticular formation of the brainstem, in the medial thalamus and, more laterally, among the posterior group nuclei and the suprageniculate nucleus. Bradykinin did not evoke any cortical or subcortical slow potentials such as those evoked by electrical stimulation of the foot pads. When bradykinin was given together with the electrical stimulus, the responses evoked by the latter were blocked.Morphines uppressed bradykinin-evoked activity. Aspirin caused marked fluctuations in activity, unrelated to the bradykinin injection; the bradykinin block of evoked potentials could no longer be observed after aspirin dosage. The results are discussed in terms of the peripheral and central sites of analgesic action and the likelihood of the existence of chemosensitive pain receptors.     

Interaction of sensory responses with spontaneous depolarization in layer 2/3 barrel cortex

The rodent primary somatosensory cortex is spontaneously active in the form of locally synchronous membrane depolarizations (UP states) separated by quiescent hyperpolarized periods (DOWN states) both under anesthesia and during quiet wakefulness. In vivo whole-cell recordings and tetrode unit recordings were combined with voltage-sensitive dye imaging to analyze the relationship of the activity of individual pyramidal neurons in layer 2/3 to the ensemble spatiotemporal dynamics of the spontaneous depolarizations. These were either brief and localized to an area of a barrel column or occurred as propagating waves dependent on local glutamatergic synaptic transmission in layer 2/3. Spontaneous activity inhibited the sensory responses evoked by whisker deflection, accounting almost entirely for the large trial-to-trial variability of sensory-evoked postsynaptic potentials and action potentials. Subthreshold sensory synaptic responses evoked while a cortical area was spontaneously depolarized were smaller, briefer and spatially more confined. Surprisingly, whisker deflections evoked fewer action potentials during the spontaneous depolarizations despite neurons being closer to threshold. The ongoing spontaneous activity thus regulates the amplitude and the time-dependent spread of the sensory response in layer 2/3 barrel cortex.     

The repeat reliability of somatosensory evoked potentials

The test-immediate-retest reliability of latency and amplitude values of cervical and cortical somatosensory evoked potentials (SEP) to median nerve stimulation was assessed in 86 normal subjects aged 15 to 71 years. In addition to the stability of data between repeat trials within one test session the standard errors of measurement and the interpretable differences for SEP measures were calculated according to measurement theory. The study revealed retest correlations rtt greater than 0.80 for all latency measures of the cervical and cortical SEPs and all cortical amplitude parameters. The highest stability was found for the latency measures of the cervical components P10, N11, N13, the cortical components P16 and N20 and for the amplitude N20/P25.     

Effect of hypothermia on median nerve somatosensory evoked potentials

Median nerve sornatosensory evoked potentials (SEP) were monitored in ten patients undergoing cardiac surgery with hypothermic cardiopulmonary bypass (CPB). Anesthesia was induced and maintained with sufentanil, oxygen, and pancuronium. Esophageal, nasopharyngeal, rectal, and blood temperatures were continuously monitored. SEPs were recorded before induction of anesthesia, after induction, and during cooling and rewarming on CPB. There was a strong negative correlation between SEP latencies and temperature (except rectal) (r = −.91, P < .001), for cortical latency and esophageal temperature. A decrease in esophageal temperature of 1°C resulted in an increase in SEP latency of 1 ms. There was also a weak positive correlation between evoked potential amplitude and temperature (r = .19) for cortical amplitude and esophageal temperature.     

Somatosensory cortical stimulus response evoked potentials in unilateral symptoms caused by cerebrovascular disorders or brain tumors

Comparative investigations of somatosensory evoked potentials in 23 patients with hemisyndromes following acute ischemia of the middle cerebral artery region and in 12 patients with similar hemisyndromes on the base of cerebral neoplasms revealed marked differences. Whereas in 87% of the patients with ischemic lesions the primary cortical complex of the SEP was severely altered there were similar abnormalities in only one of the patients with neoplasm. The SEP changes were not dependent on the neurologic (sensory) symptoms nor on focal or diffuse EEG abnormalities.     

Primary extinct evoked cerebral potentials in the diagnosis of brain death]

In a collective of 82 patients with the clinical signs of brain death and examination of evoked cerebral potentials the incidence of primary abolished evoked potentials was studied. The initial examination occurred at the same time after onset of disease in both groups. We found a marked correlation with the clinical course of the patients. Whereas the group with primary loss of evoked potentials mainly contained patients with intracerebral and subarachnoid hemorrhages and short survival times, the other group with primary preserved evoked potentials showed a high rate of ischemic infarctions and longer survival periods. The rate of primary abolished evoked potentials can be lowered only by routine examination at the earliest time possible. Outside of neurological intensive care units the early examination of evoked potentials is hardly possible. In these units, the EEG remains the technical examination of choice in the confirmation of brain death.     

Intracortical and corticothalamic coherency of fast spontaneous oscillations.

We report that fast (mainly 30- to 40-Hz) coherent electric field oscillations appear spontaneously during brain activation, as expressed by electroencephalogram (EEG) rhythms, and they outlast the stimulation of mesopontine cholinergic nuclei in acutely prepared cats. The fast oscillations also appear during the sleep-like EEG patterns of ketamine/xylazine anesthesia, but they are selectively suppressed during the prolonged phase of the slow (<1-Hz) sleep oscillation that is associated with hyperpolarization of cortical neurons. The fast (30- to 40-Hz) rhythms are synchronized intracortically within vertical columns, among closely located cortical foci, and through reciprocal corticothalamic networks. The fast oscillations do not reverse throughout the depth of the cortex. This aspect stands in contrast with the conventional depth profile of evoked potentials and slow sleep oscillations that display opposite polarity at the surface and midlayers. Current-source-density analyses reveal that the fast oscillations are associated with alternating microsinks and microsources across the cortex, while the evoked potentials and the slow oscillation display a massive current sink in midlayers, confined by two sources in superficial and deep layers. The synchronization of fast rhythms and their high amplitudes indicate that the term "EEG desynchronization," used to designate brain-aroused states, is incorrect and should be replaced with the original term, "EEG activation" [Moruzzi, G. & Magoun, H.W. (1949) Electroencephalogr. Clin. Neurophysiol. 1, 455-473].     

Somatosensory evoked potentials in moderate hyperthermia]

The effects of moderate whole-body hyperthermia on the cervical and cortical somatosensory evoked potentials (SEP) were studied in healthy male subjects, aged 22-32 years. They were immersed in hot water and heated to a median rectal temperature of 39.0 degrees C. Serial SEPs to median nerve stimulation were recorded during cooling at intervals of 0.1 degrees C. The general wave form and the amplitudes did not systematically change. For a 1 degrees C drop there was a median latency increase of 2.6-3.7% in cervical and 1.5-7.4% in cortical SEP components. In individual cases significant latency delays of cervical N13 and cortical N20 could already be observed at differences of 0.2 degrees and 0.5 degrees respectively. All other components showed significant latency changes at temperature intervals of 0.6 to 0.8 degrees C.