Sadahei Denda

Effects of Isoflurane on Spinal Inhibitory Potentials

The effects of isoflurane on segmental spinal cord potentials and heterosegmental slow positive potentials in response to fore- and hindpaw stimulation were studied in the rat. The heterosegmental slow positive potential and late (second) component of the slow positive wave (P2) of segmental spinal cord potential, thought to be primary afferent depolarization, an agent of presynaptic inhibition activated by a feedback loop via supraspinal structures, were greatly suppressed by the anesthetic. In contrast the negative wave (N1) of segmental spinal cord potential, believed to be synchronized activity of dorsal horn neurons, was only minimally affected. No differential effects of isoflurane on spinal cord potentials activated by fore- and hindpaws were found. Thus, the inhibitory activities of the spinal cord, particularly those produced by a feedback loop via supraspinal structures, are suggested to be highly vulnerable to isoflurane.

Slow positive dorsal cord potentials activated by heterosegmental stimuli

Heterosegmental slow positive waves (HSPs) and segmental spinal cord potentials were recorded from the cord dorsum in ketamine-anesthetized rats. Forepaw stimulation produced HSPs in the lumbo-sacral enlargement (lumbar HSPs), whereas hind paw stimulation evoked HSPs in the cervical cord (cervical HSP). Both the HSP and the secondary component of the slow positive wave (P2s) in the segmental spinal cord potential were highly vulnerable to anesthetics and completely disappeared after spinal cord transection at the C1/2 level, indicating that both the HSP and P2s are produced by a long feedback loop via supraspinal structures. The lumbar HSP evoked by forepaw stimulation was maximal in amplitude at the L5 level and more dominant in the ipsilateral cord dorsum than in the contralateral one, but widely distributed in the lumbo-sacral cord. A variability of onset (7-18 msec for cervical and 5-17 msec for lumbar HSPs) and peak (22-35 msec for cervical and 12-50 msec for lumbar HSPs) suggests the existence of several nuclei to form the feedback loops for descending impulses to produce the HSPs. There were no peak latency differences between the HSPs and P2s. Since there were several similar characteristics between the P2s and HSP such as a high vulnerability to anesthetic, a complete disappearance after high spinal transection and similar response curves to graded intensities of stimulation, there may be a close relationship between their feedback nuclei and the pathways mediating them. All wide dynamic range (WDR) neurons (12/12) in lamina V of Rexed responded to heterosegmental stimulation with inhibition of firing.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of dorsal root entry zone lesion on spinal cord potentials evoked by segmental, ascending and descending volleys

SummaryThe spinal cord potentials (SCPs) were recorded from the dorsal root entry zone (DREZ) and posterior epidural space in patients before and after dorsal root entry zone lesion (DREZL) during general anaesthesia. The SCPs from the DREZ activated by segmental, ascending and descending volleys were basically the same in fundamental waveform as those recorded from the posterior epidural space. Segmentally activated slow negative (N1) wave, reflecting synchronized activities of dorsal horn neurones, and positive (P2) wave, thought to indicate primary afferent depolarization, were affected by DREZL in all 4 subjects tested, even by contralateral stimulation, suggesting that these components of the segmental SCPs in man partly reflect the activities of the contralateral dorsal horn. The spike-like potentials activated by ascending volleys were not affected by DREZL, while the subsequent slow components were decreased in the lesioned level. This may indicate that ascending spinal cord tracts are not affected by the operation, and suggests that the origin of the slow components by ascending volleys lies at least in part in the segmental dorsal horn. The slow negative and positive components, recorded at a remote segment from DREZL, in response to the descending volleys, were augmented after DREZL, suggesting that activation of ascending or descending inhibition through a feedback loop via the supraspinal structures might occur at least transiently following DREZL. All components of the SCPs activated by descending volleys were decreased or disappeared in recording from the lesioned level, as expected. Thus, intra-operative recording of the SCPs during DREZL might be beneficial for monitoring and studying human spinal cord function.

Spinal tracts producing slow components of spinal cord potentials evoked by descending volleys in man

Slow negative (N) and slow positive (P) waves are frequently produced in the posterior epidural space at the lumbosacral enlargement by epidural stimulation of the rostral part of human spinal cord. The production of these slow potentials are thought to be responsible for analgesia at the stimulated segment as well as below that level. In order to define the spinal tract which mediates these slow potentials, we stimulated directly or from the epidural space the dorsal, dorsolateral, lateral and ventral columns at the cervical or thoracic level, and epidurally recorded spinal cord potentials (des.SCPs) at the lumbosacral enlargement in 7 patients who underwent spine or spinal cord surgery. The des.SCPs recorded in the lumbosacral enlargement consisted of polyphasic spike potentials followed by slow N and P waves. At a near threshold level of stimulus intensity the slow N and P potentials were consistently elicited only by stimulation of the dorsal column. The slow waves were also produced by intense stimulation of other tracts, but remained significantly (P < 0.05 - P < 0.01) smaller than those evoked by dorsal column stimulation when compared at the same stimulus intensity. Moreover, the slow P wave could not be elicited even by intense stimulation (10 times the threshold strength for the initial spike potentials) of the ventral column. Thus, the results suggest that the slow N and P waves are mostly mediated by the antidromic impulses descending through the dorsal column.

Effects of Pentobarbital on Heterosegmentally Activated Dorsal Root Depolarization in the Rat Investigation by Sucrose-gap Technique In Vivo

Slow positive cord dorsum (P-) potentials activated by segmental stimulation are believed to reflect primary afferent depolarizations and have been shown to be augmented by barbiturates. However, there have been no data to confirm whether heterosegmentally activated P-potentials also represent primary afferent depolarizations and are similarly affected by barbiturates. We therefore tested whether heterosegmental P-potentials reflect primary afferent depolarizations and how these heterosegmental potentials are affected by barbiturates. Heterosegmentally activated dorsal root (DR) depolarizations (depolarizations evoked in DRs of lumbar segments in response to afferent volleys to cervical segments produced by electrical stimulation of the forepaw) and P-potentials were simultaneously recorded, adapting the sucrose-gap technique for recording DR depolarization in vivo in the rat. Forepaw (heterosegmental) stimulations produced a large depolarization in the DRs of L5-S1 as well as a slow P-potential in the lumbosacral enlargement. Transection of the spinal cord at the level of C1-C2 abolished both the P-potential and DR depolarization activated by heterosegmental stimulation as well as the second component of segmentally (hind-paw) activated P-potential. Bicuculline (100 micrograms/kg, intravenous) augmented the P-potential and DR depolarization produced by heterosegmental stimulation, but larger doses, 400-600 micrograms/kg, eventually suppressed these. However, the drug, in a dose-dependent manner, suppressed both the P-potential and DR depolarization produced by the segmental stimulation. Pentobarbital (10-40 mg/kg, intravenous) suppressed in a dose-dependent manner both the heterosegmental P-potential and heterosegmental DR depolarization and prolonged their peak latencies. By contrast, pentobarbital augmented and prolonged the segmental P-potential and segmental DR depolarization.(ABSTRACT TRUNCATED AT 250 WORDS)

Somatosensory evoked potentials recorded from the posterior pharynx to stimulation of the median nerve and cauda equina

Somatosensory evoked potentials (ppSEPs) in response to stimulation of the median nerve at the wrist and the cauda equina at the epidural space (the L4 level) were recorded from the posterior wall of the pharynx in 15 patients who underwent spinal surgery under general anesthesia, using disc electrodes attached to the endotracheal tube, and compared with segmental spinal cord potentials (seg-SCPs) that were recorded simultaneously from the posterior epidural space (PES). ppSEPs consisted of the initially positive spike (P9) followed by slow positive (P13) and negative (N22) waves. The P13 and N22 of ppSEPs had phase reversal relationship with the P2 and N2 recorded from the PES, respectively. The peak latencies of P9 (9.40 +/- 0.7 ms) (mean +/- SD), P13 (13.1 +/- 0.9 ms), and N22 (22.0 +/- 2.1 ms) of ppSEPs coincided with those of P1, N1 and P2 of seg-SCPs, respectively, ppSEPs were recorded more clearly with a reference electrode on the dorsal surface of the neck than with the reference electrode at the earlobe or back of the hand. The threshold and maximal stimulus intensities were also similar between the ppSEPs and seg-SCPs. Thus, the P9, P13, and N22 components of ppSEPs were thought to have the same origin as the P1, N1 and P2 of seg-SCPs, respectively. Therefore, the P9, P13 and N22 of ppSEPs may reflect incoming volleys through the root, synchronized activities of the interneurons and primary afferent depolarizations (PAD), respectively. ppSEPs in response to cauda equina stimulation showed that the latencies of the two initial components (4.6 +/- 0.4 and 6.4 +/- 0.6 ms) corresponded to those of the SCPs recorded from the PES (4.6 +/- 0.3 and 6.3 +/- 0.5 ms), suggesting that these potentials reflect impulses conducting through the spinal cord, similar to epidurally recorded SCPs.

Tolerance to N2O-induced alterations in somatosensory evoked potentials.

Summary The effect of nitrous oxide (N2O) on somatosensory evoked potentials from the cortical (CEP) and spinal cord (SCP) regions in response to forepaw stimulation was studied in ketamine-anesthetized and mechanically ventilated rats. The CEP was recorded from the skull over the contralateral somatosensory area; the SCP was recorded from the supraspinous ligament at C57–6 and L1-2 levels of the spine. Rats were exposed to 70% N2O for 5 h, whereupon N2O was withdrawn for 2 h. Thereafter, the rats were re-exposed to N2O for 10 min. The N13-P21 component of the CEP, the slow positive wave (P2) of the segmental SCP, and the heterosegmental positive cord dorsum potential (HSP) were significantly suppressed by N2O, while the large negative (N1) component of the segmental SCP remained unchanged. A partial recovery of the CEP and HSP was observed during the 5 h of N2O anesthesia, while significant recovery of the P2 component of the SCP was not observed. The withdrawal from N2O following 5 h exposure caused an augmentation of the CEP (When compared to the control values). Re-exposure of rats to N2O again caused the suppression of these potentials as in the initial exposure. The results suggest that the phenomenon of tolerance to N2O in terms of evoked potentials develops within 5 h in the brain but not in the spinal cord.

Transcranial Electrically Evoked SCPs (TCE-Evoked SCPs)

Even with the use of microsurgical techniques, neurosurgery on the spinal cord involves high risk for serious neurological complications. Over the past five to ten years, neurophysiological monitoring techniques have become increasingly popular, aiming to prevent intraoperative neurological impairment. Several types of evoked spinal cord potential in human subjects have been reported. These have provided hope that spinal cord functions can be assessed objectively by neurophysiological monitoring during surgery.