Monitoring somatosensory evoked potentials in spinal cord ischemia-reperfusion injury*******

Transcription

1 NEURAL REGENERATION RESEARCH Volume 8, Issue 33, November doi: /j.issn [ Ji YM, Meng B, Yun CX, Yng HL, Zou J. Monitoring somtosensory evoked potentils in spinl cord ischemi-reperfusion injury. Neurl Regen Res. 2013;8(33): Monitoring somtosensory evoked potentils in spinl cord ischemi-reperfusion injury******* Yiming Ji, Bin Meng, Chenxi Yun, Huilin Yng, Jun Zou Deprtment of Orthopedic Surgery, the First Affilited Hospitl of Soochow University, Suzhou , Jingsu Province, Chin Reserch Highlights (1) Intropertive monitoring of somtosensory evoked potentils is regrded new mesure to void itrogenic spinl cord injury. (2) This study is chrcterized by tht, through the chnges of somtosensory evoked potentil ltency in the rbbit spinl cord ischemi-reperfusion injury, we cn confirm the objective quntittive monitoring efficcy of somtosensory evoked potentils in the ssessment of spinl functions. Abstrct It remins uncler whether spinl cord ischemi-reperfusion injury cused by ischemind other non-mechnicl fctors cn be monitored by somtosensory evoked potentils. Therefore, we monitored spinl cord ischemi-reperfusion injury in rbbits using somtosensory evoked potentil detection technology. The results showed tht the somtosensory evoked potentil ltency ws significntly prolonged nd the mplitude significntly reduced until it disppered during the period of spinl cord ischemi. After reperfusion for minutes, the mplitude nd ltency begn to grdully recover; t 360 minutes of reperfusion, the ltency showed no significnt difference compred with the pre-ischemic vlue, while the somtosensory evoked potentil mplitude incresed, nd severe hindlimb motor dysfunctions were detected. Experimentl findings suggest tht chnges in somtosensory evoked potentil ltency cn reflect the degree of spinl cord ischemic injury, while the mplitude vritions re indictors of the lte spinl cord reperfusion injury, which provide evidence for the ssessment of limb motor function nd void itrogenic spinl cord injury. Key Words neurl regenertion; spinl cord injury; somtosensory evoked potentils; spinl cord; ischemi; reperfusion; itrogenic spinl cord injury; histopthology; bdominl ort occlusion model; ltency; grnts-supported pper; neuroregenertion Yiming Ji, Ph.D., Associte chief physicin. Corresponding uthor: Jun Zou, Ph.D., Attending physicin, Deprtment of Orthopedic Surgery, the First Affilited Hospitl of Soochow University, Suzhou , Jingsu Province, Chin, jzou@sud.edu.cn. Received: Accepted: (N ) Funding: This study ws supported by the Ntionl Nturl Science Foundtion of Chin, No , , ; the Nturl Science Foundtion of Jingsu Province in Chin, No. BK ; Jingsu Province Science nd Technology Support Progrm (Socil Development) in Chin, No. BE ; University Nturl Science Reserch Foundtion of Jingsu Province for Higher Eduction, No. 12KJB320008; College Grdute Reserch nd Innovtion Pln of Jingsu Province in Chin, No. CXZZ11_0126. Author contributions: Zou J nd Yng HL were responsible for the study concept nd design. Ji YM, Meng B, nd Yun CX were in chrge of dtnlysis nd writing of the mnuscript. Zou J supervised the study nd performed sttisticl nlysis. All uthors pproved the finl nlysis of the mnuscript. 3087

2 Conflicts of interest: None declred. Ethicl pprovl: This study ws pproved by the Animl Ethics Committee of Soochow University, Chin. Author sttements: The mnuscript is originl, hs not been submitted to or is not under considertion by nother publiction, hs not been previously published in ny lnguge or form, including electronic, nd contins no disclosure of confidentil informtion or uthorship/ptent ppliction/funding source disputtions INTRODUCTION The rpid development of spinl surgery technologies nd instruments llow for the surgicl tretment of ptients with spinl cord disorders, tumors nd mlformtions, who hve hd no surgery for some time [1-4]. However, spinl surgery itself cn cuse dmge through reperfusion injury, even if the surgery is very fine nd delicte. Thus, the prevention of itrogenic spinl cord reperfusion injury remins n urgent problem. Somtosensory evoked potentil is response of the nervous system to outside specific stimuli nd n indictor of detecting neurl pthwy integrity. In the middle of the 1980s, some scholrs hve successfully pplied somtosensory evoked potentils for intropertive monitoring of spinl cord functions [2]. In ddition, the combintion of somtosensory evoked potentils nd motor evoked potentils significntly improved the prediction ccurcy of spinl cord functions [3-4], thus gretly reducing the incidence of itrogenic spinl cord injury. Currently intropertive monitoring using somtosensory evoked potentils hs been widely recognized to prevent itrogenic spinl cord injury [2] due to simple opertion, stble signls of intropertive monitoring, nd no influence on opertion. Previous studies only reported the monitoring effects of somtosensory evoked potentils fter mechnicl fctors-cused spinl cord injury [1-4]. However, spinl cord injury is not only triggered by mechnicl fctors, biochemicl fctors nd vsculr fctors my cuse spinl cord ischemi-reperfusion injury. Spinl cord ischemi-reperfusion injury is the result of lipid peroxidtion, excessive free rdicls, leukocyte ctivtion, relese of inflmmtory meditors nd other pthophysiologicl mechnisms [5-8]. After the compression of spinl cord nerve cells during the ischemi-reperfusion period, some injury fctors my led to pprent limb dysfunction nd even irreversible delyed neuronl deth, ultimtely leding to prlysis, even though the compressed nerve cells my regin blood reperfusion. In summry, this study ims to observe the chnges in somtosensory evoked potentils during spinl cord ischemi-reperfusion injury nd to investigte the functions of somtosensory evoked potentils on monitoring spinl cord functions. RESULTS Quntittive nlysis of experimentl nimls Thirty New Zelnd rbbits were used in this study. Twenty-four of the rbbits were rndomly divided into three groups, in which the bdominl ort ws occluded for 20, 30, or 40 minutes, respectively, fter spinl cord ischemi-reperfusion injury models were estblished. Subsequently, somtosensory evoked potentil ltency nd mplitude were monitored nd recorded before occlusion, during occlusion nd t 30, 60, 120, 180, 240, 300, nd 360 minutes fter reperfusion. The remining six rbbits served s the controls, three of which were used s the norml control group, while the remining three were scrificed t 40 minutes fter bdominl ort occlusion to observe histologicl chnges in the spinl cord. Finlly, ll 30 rbbits were involved in the finl nlysis. Chnges of somtosensory evoked potentils during spinl cord ischemi-reperfusion injury in rbbits Norml somtosensory evoked potentil wveforms were detected immeditely fter the rbbit skin ws sutured under nesthesi, including N-wve nd P-wve in both positive nd negtive phses. After the rbbit bdominl ort ws occluded, the somtosensory evoked potentil mplitude decresed grdully nd the ltency period grdully prolonged. After the bdominl ort ws occluded for 7 15 minutes, the mplitude reduced by pproximtely 50%, nd somtosensory evoked potentil wveforms disppered t 20.0 ± 7.3 minutes. The potentil disppernce occurred from 5 35 minutes fter occlusion.

3 L2 (ms) L1 (ms) Ji YM, et l. / Neurl Regenertion Reserch. 2013;8(33): The reperfusion procedure refers to the occlusion, unclmping nd reocclusion of the bdominl ort in New Zelnd white rbbits. Somtosensory evoked potentils my grdully restore fter reperfusion, 3 11 minutes fter the removl of the clmp. After reperfusion, the ltency of somtosensory evoked potentils (N-wve pek time nd P-wve trough time) grdully returned to ner norml levels (P < 0.05; Figures 1, 2). At 360 minutes fter reperfusion, the ltency showed no significnt difference compred with the norml levels before ischemi (P > 0.05). The mplitude of somtosensory evoked potentils begn to decrese during the spinl cord ischemi period (dt not shown, only chnges were recorded), then grdully incresed during the erly reperfusion period ( minutes), nd begn to decline during the lte reperfusion period ( minutes; Tble 1). Tble 1 Chnges of somtosensory evoked potentil mplitudes (%) in rbbits with spinl cord ischemireperfusion injury Group Norml Reperfusion 30 min Reperfusion 60 min Reperfusion 120 min Reperfusion 180 min Reperfusion 240 min Reperfusion 360 min 20 min fter occlusion min fter occlusion min fter occlusion The vritions of somtosensory evoked potentil mplitudes re clculted s follows: mplitude fter modeling/mplitude of norml rts 100%, n = eight rbbits per time point of occlusion. Somtosensory evoked potentil mplitudes of rbbits in ech group begn to increse t minutes (min) fter reperfusion, nd then grdully decresed t reperfusion min Ischemi 20 min Ischemi 30 min Ischemi 40 min Norml Time of occlusion (min) Correltion between somtosensory evoked potentil ltency, mplitude nd hindlimb motor function fter spinl cord ischemi-reperfusion There were no sttisticlly significnt differences in somtosensory evoked potentil ltencies mong groups fter spinl cord ischemi-reperfusion. At 360 minutes fter reperfusion, the rbbit hindlimbs exhibited severe motor dysfunction, where the mplitude decresed shrply. Figure 1 N-wve pek time (L1) of somtosensory evoked potentil ltency in rbbits with spinl cord ischemi-reperfusion injury. P < 0.05, vs. norml stte before occlusion. Dtre expressed s men ± SD, n = eight rbbits per time point of occlusion, one-wy nlysis of vrince nd lest significnt difference test. min: Minutes. Hindlimb motor dysfunction ws not visible in rts with mplitude chnge > 44%, but becme severe in rts with mplitude vrition < 35% (Tble 2). The N-wve pek time (L1) nd P-wve trough time (L2) of rts in ech group prolonged with incresed severity of hindlimb dysfunction Norml Figure 2 P-wve trough time (L2) of somtosensory evoked potentil ltency in rbbits with spinl cord ischemi-reperfusion injury. P < 0.05, vs. norml stte before occlusion. Dtre expressed s men ± SD, n = eight rbbits per time point of occlusion, one-wy nlysis of vrince nd lest significnt difference test. min: Minutes. Time of occlusion (min) Ischemi 20 min Ischemi 30 min Ischemi 40 min Spinl cord tissue pthologicl chnges fter spinl cord ischemi-reperfusion Spinl nerve cells were complete, with cler nuclei, dendrites nd xons in the norml control group (Figure 3A). At 40 minutes fter bdominl ort occlusion, spinl nerve cells were lightly stined, the nuclei dissolved nd were bsent, with perinucler hlos (Figure 3B). At 360 minutes fter reperfusion, spinl nerve cell edem ws visible, the gp between cells widened significntly, the polrity ws blunt nd there were uncler nuclei boundries. Furthermore, neutrophils were scttered within the tissues, some neurons hd degenerted nd becme necrotic, with vcuoliztion nd pprent hemorrhge, nd lrge number of neurons hd bnorml morphologies (Figure 3C). 3089

4 Tble 2 Chnges of somtosensory evoked potentil ltency, mplitude nd hindlimb motor function t 360 minutes in rbbits with spinl cord ischemi/reperfusion injury Group Hindlimb motor function grde n N-wve pek time (L1, men±sd, ms) P-wve trough time (L2, men±sd, ms) Amplitude (%) 20 min occlusion I II III 30 min occlusion I II III 40 min occlusion I II III ± ± ± ± ± ± ± ± ± ± ± ± ± ± Somtosensory evoked potentil ltencies L1 nd L2 re incresed s the severity of hindlimb dysfunction. At 360 minutes (min) of reperfusion, the mplitude decresed shrply in the rbbit hindlimbs, where severe motor dysfunction ws observed. There re eight rbbits per time point of occlusion. Hindlimb motor function evlution criteri (self-mde): level I: norml motor nd sensory stte (no spontneous hindlimb ctivity, with ctivity in both hips nd toes identifible fter stimultion); level II: moderte motor nd sensory loss (flccid prlysis on one side, or only nkle movement, or mild ctivity on one side fter stimultion); level III: severe motor nd sensory loss (no bilterl limb movement fter stimultion). A B C Figure 3 Spinl cord tissue t 360 minutes in rbbits with spinl cord ischemi-reperfusion injury (hemtoxylin-eosin stining, opticl microscopy, 100). (A) In the norml control group, spinl nerve cells showed complete structure. (B) At 40 minutes fter bdominl ort occlusion, the nuclei of spinl nerve cells hd dissolved nd disppered. (C) At 360 minutes fter reperfusion, spinl nerve cell edem ws observed, nucler boundries were uncler, nd some cells degenerted nd becme necrotic, with pprent hemorrhge loci. DISCUSSION Somtosensory evoked potentils were first proposed by Tmki nd Nsh [9-10] s n effective electrophysiologicl mens for monitoring spinl cord functions, nd hs been widely used in vrious types of surgery involving neurologicl dmge; however, few reports hve been published in Chin. Somtosensory evoked potentils cn record bnorml chnges in skin round the surgicl re through stimulting mixed peripherl nerves. Stimulting electrodes re often plced t the posterior tibil nerve, peronel nerve, femorl nerve, nd surl nerve. The stimultion cn be given t μs squre wve, stimuli per second. The stimuli intensity ssocited with the stimultion electrode is generlly ma. Recording electrodes re plced round the surgicl incision, somtosensory cortex nd subcortex. Somtosensory evoked potentils re usully evoked by peripherl sensory nerve fibers in the centrl nervous system under continuous stimultion; its vritions my reflect the severity of spinl sensory nerve dysfunction, nd it is n objective, quntittive nd sensitive indictor for sensory dysfunction. The spinl cord dorsl funiculus nd posterior lterl funiculus re the min pthwy for somtosensory evoked potentil conduction [10]. The occurrence of somtosensory evoked potentils depends on the integrity of the ipsilterl spinl cord dorsl funiculus nd posterolterl funiculus, nd it cn reflect spinl sensory conduction pthwy function, especilly fter spinl cord ischemi- reperfusion injury. Spinl cord nterior nd posterior funiculi re djcent to ech other nd cn be entrpped by the sme spinl pi mter, so somtosensory evoked potentils indirectly reflect the function of the nterior funiculus. This evidence indictes correltion between somtosensory evoked potentils nd hindlimb motor function, thus providing indirect demonstrtion for hindlimb motor function. Currently, the monitoring of somtosensory evoked potentils is regrded s n importnt mens for the dignosis of spinl cord injury nd evlution of spinl cord function. The gols of intropertive monitoring of evoked potentils re fivefold: first, to determine cute injury severity nd loction in the neurl conduction pthwy, thus promptly correcting induction fctors; second, to quickly observe cute systemic chnges, such s hypotension; third, to define nerve tissue round or within the tumor; fourth, to llow surgery in high-risk ptients; nd fifth, to ensure the implementtion of more extensive surgicl 3090

5 procedures performed on ptients [11]. Ki et l [12] proposed the min cuses for spinl cord injuries s both structurl nd vsculr injury. Somtosensory evoked potentils re the dominnt mens for detecting sensory pthwys, but the surgeons focus their observtions on motor function. Becuse the motor pthwy is similr to the sensory pthwy in ntomy, dmge to motor function indirectly ffects sensory responses fter mechnicl injury. As for spinl cord injury cused by vsculr fctors, the motor nd sensory pthwys hve different blood supply sources, so no sensory dysfunction occurs even though motor dysfunction cn be detected. In spinl surgery, surgeons often py more ttention to preventing structurl dmge, while potentil vsculr injury my be ignored. The gol of this study is to comprehensively reflect the chnges of somtosensory evoked potentils fter spinl cord ischemind reperfusion. The results showed tht, fter the rbbit bdominl ort ws clmped, somtosensory evoked potentil ltencies grdully prolonged nd the mplitude grdully decresed s time proceeded. After reperfusion, both the mplitude nd ltency grdully returned to norml levels, but the mplitude begn to reduce during the lte reperfusion period. An evoked potentil mplitude is determined by the number of neurons nd the response synchroniztion, while the ltency is closely ssocited with the conduction velocity [13-17]. Nerve conduction is ffected by myelin function of myelinted nerve fibers. Ischemi cn slow conduction velocity nd produce trnsient nerve block, resulting in prolonged ltency. After reperfusion, myelin functions nd conduction velocity grdully restored, nd ccordingly the ltency lso returns to norml. The mplitude restored during erly reperfusion nd then decresed during the lte reperfusion period, which corresponded with ggrvted limb dysfunction, suggesting tht chnges in mplitude reflect the secondry injury fter reperfusion. In this study, we found tht one rbbit recovered motor function, which is possibly due to individul differences, where its spinl cord my not hve been sensitive to ischemi. Somtosensory evoked potentils cn reflect the integrity of the spinl cord dorsl funiculus pthwy [18-20]. Structurl dmge cused by mechnicl fctors directly ffects the integrity of the posterior funiculus pthwy, nd thus somtosensory evoked potentils cn be pplied to monitor spinl cord functions nd spinl cord injury cused by ischemind other non-mechnicl fctors, with the following possible mechnisms: (1) After bdominl ort is occluded, locl blood supply redistributes to form stel blood phenomenon. Abdominl ort clmping results in severe blood supply insufficiency in the nterior spinl rtery, lso ffecting blood supply in the posterior spinl rtery, which compenstively trnsfers blood into the nterior spinl rtery, resulting in chnges in spinl cord dorsl funiculus function nd somtosensory evoked potentils. After the bdominl ort clmp ws relesed, blood supply in the nterior spinl rtery ws restored, nd no compenstory blood supply of the posterior spinl cord rtery ws required, the blood supply of the posterior spinl rtery ws then restored nd somtosensory evoked potentils underwent corresponding recovery. (2) It is generlly recognized tht the conduction of somtosensory evoked potentils is chieved through the posterior funiculus, where the dorsl root gngli xons enter the spinl cord, trvel long the ipsilterl fsciculus grcilis nd fsciculus cunetus, nd cross into the medull oblongt. This non-synptic conduction pttern hs been confirmed to be strongly tolernt ginst ischemind cn consume less energy. The lbeling results of blood flow showed tht short-term ischemi cnnot induce loss of function in non-synptic conduction pthwys, nd so the ltency of somtosensory evoked potentils grdully returned to norml fter blood supply ws restored. (3) In contrst, synptic conduction pthwys require gret energy nd re sensitive to ischemi. Moreover, in sensory conduction pthwys, both spinl cord posterior funiculus nd gry mtter second-grde neurons re involved in the conduction of somtosensory evoked potentils. These second-grde neurons re lso sensitive to ischemi nd my become necrotic fter long-term ischemi. Somtosensory evoked potentil mplitudes re lrgely dependent on the number of neurons nd the response synchroniztion. The decline of neuronl number my trigger reduction in mplitude. (4) After spinl cord ischemi-reperfusion, excittory mino cids (glutmic cid, sprtic cid, folic cid) nd intrcellulr C 2+ content in spinl cord tissue increse, s well s their resultnt cscde rections, leding to xonl degenertion nd neuronl necrosis, which ply decisive role on ischemi-reperfusion injury. This could lso be explined by the mplitude increse t erly reperfusion nd decline t lte reperfusion [21-24]. At 360 minutes fter reperfusion, hindlimb function evlution results showed tht limb dysfunction hd no pprent correltion with somtosensory evoked potentil ltency, nd there ws no significnt difference in the ltency compred with pre-ischemi levels, lthough loss of motor nd sensory function ws severe. This evidence 3091

6 indictes tht restortion of somtosensory evoked potentil ltency cnnot represent the synchronous recovery of spinl cord function, in prticulr motor function, becuse the pyrmidl trcts, which re responsible for the conduction of motor function, re locted in the nterior spinl cord nd supplied by the nterior spinl rtery. Our findings re consistent with previous studies [25-26], which found tht intropertive somtosensory evoked potentils were norml in ptients with the development of lower limb dysfunction fter spinl surgery. This evidence lso indictes tht posterior spinl rtery injury cn be reversed, while nterior spinl rtery injury is irreversible. In prticulr, the posterior funiculus itself hs strong tolernce ginst ischemi. Myelin hs the bility to regenerte nd, s myelin function ffects conduction velocity, it lso ffects somtosensory evoked potentil ltency. Moreover, s ischemi induces chnges in myelin function, it lso slows conduction velocity nd prolongs the ltency. After reperfusion, myelin functions nd conduction velocity restore, nd ccordingly the ltency lso returns to norml; however, pthologicl chnges cused by prolonged ischemi-induced neuronl necrosis re irreversible. In this study, when spinl cord ischemi cused neuronl necrosis, the number of neurons involved in the trnsduction nd synchroniztion response reduced, resulting in decrese in evoked potentil mplitude. Moreover, t 6 hours fter reperfusion, severe hindlimb motor disorders were observed in rts with mplitudes < 35%, while it ws not present in rts with mplitudes > 44%. These discrepncies provide criteri for determining the severity of spinl cord ischemi following reperfusion nd for ssying hindlimb motor function. After 2 3 hours of reperfusion, somtosensory evoked potentil mplitudes reduced further, suggesting the potentil occurrence of reperfusion injury. At this time some protective mesures my reduce spinl cord injury. The representtive imges in Figure 3 pper s though the nerves re helthier t 360 minutes thn t 40 minutes. This could be due to vritions in the procedure. In summry, we believe tht somtosensory evoked potentils re sensitive indictor for monitoring spinl cord ischemi-reperfusion injury, in which chnges in ltency reflect spinl cord ischemic insult, while chnges in mplitude reflect lte reperfusion injury. When the somtosensory evoked potentil mplitude remins unchnged nd the ltency chnges gretly, only myelin tissue is dmged; when both the mplitude nd ltency exhibit vritions, the centrl nervous system is lso ffected. Therefore, somtosensory evoked potentils re n indirect mens to determine the position of nerve tissue necrosis nd to predict the prognosis following spinl cord injury. Our experimentl findings indicte tht there ws no pprent correltion between the vritions of somtosensory evoked potentil ltency nd the restortion of spinl cord function. This evidence indictes tht somtosensory evoked potentils nd motor evoked potentils should be monitored simultneously to comprehensively determine spinl cord function nd reduce the incidence of intropertive monitoring flse negtivities nd flse positives. MATERIALS AND METHODS Design A rndomized, controlled niml experiment. Time nd setting The experiment ws performed from Jnury 2011 to Jnury 2012 t Orthopedic Lbortory, the First Affilited Hospitl of Soochow University, Chin. Mterils Thirty helthy New-Zelnd white rbbits, of either gender, weighing ± 500 g, were purchsed from the Experimentl Animl Center of Soochow University, Chin (license No. SYXK (Su) ). Experimentl disposls were in ccordnce with the Guidnce Suggestions for the Cre nd Use of Lbortory Animls, issued by the Ministry of Science nd Technology of Chin [27]. Methods Estblishment of spinl cord ischemi/reperfusion injury models Spinl cord ischemi/reperfusion injury models were estblished s previously described [28-29]. In brief, rts were nesthetized with 25% urethne (4 ml/kg), injected into the uriculr vein. Rbbits were fixed on the operting tble under nesthesi, the skull hir ws removed nd the operting field ws routinely disinfected. A left lterl incision ws then mde sterilely nd somtosensory evoked potentils were monitored nd recorded immeditely. The skin nd muscle were cut open long the prspinl muscles. After the position of left renl rtery ws determined, the tissue ws bluntly dissected vi the retroperitonel spce. The bdominl ort ws exposed nd blocked cm below the left renl rtery, until rteril pulstion below the blocking site completely disppered, indicting the success of occlu- 3092

7 sion. The blood flow ws blocked for certin periods nd then relesed, following which the incision ws sutured. Somtosensory evoked potentils were continuously monitored during the occlusion procedure, nd ech rbbit ws covered with wrm sline guze on orgns nd incisions. The room temperture ws mintined t C. Implnttion of somtosensory evoked potentils stimulting electrodes nd recording electrodes nd recording of stimultion prmeters The vritions of somtosensory evoked potentils were observed with Viking IV type evoked potentil pprtus (Thermo Nicolet Corportion, Mdison, WI, USA). Electricl stimultion ws t pulse squre wve of 0.2 ms width nd 3.9 Hz frequency, nd the stimuli intensity ws permissible upon the symptoms of rbbit toe jogging. Recording electrodes were plced 17.5 mm bove the sgittl suture on the skull surfce nd 3.5 mm lterl, which ws close to hindlimb sensory projection re. Reference electrodes were plced below the sclp; signls were collected nd nlyzed through 500 superpositions with sensitivity of 5 μv, nd the filtering rnged from Hz. The ltency (L) refers to the period from the beginning of stimultion to the emergence of wve pek in milliseconds (ms) s unit. The first upwrd wve ws the N wve nd the N-wve pek (L1) ws recorded; nd the second downwrd wve ws P wve, nd the P-wve trough (L2) ws recorded. The mplitude ws mesured s the distnce from N-wve pek or P-wve trough to the bseline, in millivolts (mv) s unit. Vritions of mplitude were clculted s follows: mplitude fter modeling/mplitude in norml rts 100%. The somtosensory evoked potentils were monitored before occlusion, during occlusion, nd t 30, 60, 120, 180, 240, 300, nd 360 minutes fter reperfusion. Evlution of hindlimb motor function fter spinl cord ischemi-reperfusion The hindlimb motor function of New Zelnd white rbbits ws ssyed fter ischemi (20, 30, 40 minutes) nd reperfusion (360 minutes) ccording to the self-mde limb movement function criteris follows: level I: norml motor nd sensory stte (no spontneous hindlimb ctivity, nd ctivities of both hips nd toes re identifible fter stimultion); level II: moderte motor nd sensory loss (flccid prlysis on one side, or only nkle movement, or mild ctivity on one side fter stimultion); level III: severe motor nd sensory loss (no bilterl limb movement fter stimultion). Histologicl chnges of spinl cord fter spinl cord ischemi-reperfusion After 40-minute occlusion nd 360-minute reperfusion, the rbbits were scrificed nd spinl cord specimens were hrvested. Then specimens were fixed in 10% neutrl formlin solution for 72 hours, prffin-embedded, sliced into continuous cross-sections for hemtoxylineosin stining. The pthologicl chnges of spinl cord specimens were observed under n upright opticl microscope (Axio Imger M1, Crl Zeiss Compny, Germny). In comprison to the spinl cord tissue of norml rbbits in the control group, the histologicl chnges of injured spinl cord specimens were observed to determine the effect of ischemi. Sttisticl nlysis Mesurement dt were expressed s men ± SD nd dt were expressed s the percentge. All dt were nlyzed using SPSS 18.0 softwre (SPSS, Chicgo, IL, USA). The dt between groups were compred using one-wy nlysis of vrince nd lest significnt difference test, P < 0.05 vlue ws considered sttisticlly significnt. Reserch bckground: Intropertive monitoring using somtosensory evoked potentils hs been widely recognized s one of effective mesures for voiding itrogenic spinl cord injury, nd somtosensory evoked potentils cn directly reflect the integrity of spinl cord dorsl funiculus pthwy fter mechnicl-induced structurl dmge. Thus, we speculted tht somtosensory evoked potentils cn be pplied to monitor spinl cord function. Reserch frontiers: Previous studies minly focused on the vritions of somtosensory evoked potentils fter spinl cord injured cused by mechnicl fctors; however, little evidence is vilble regrding spinl cord ischemi-reperfusion injury cused by ischemind other non-mechnicl fctors. Clinicl significnce: Intropertive monitoring using somtosensory evoked potentils cn improve the prediction ccurcy of spinl cord function nd reduce the incidence of itrogenic spinl cord injury. Acdemic terminology: Somtosensory evoked potentils group of comprehensive potentil ctivities evoked by peripherl sensory nerve fibers in the centrl nervous system. Following continuous stimultion, chnges in somtosensory evoked potentils cn reflect the severity of spinl sensory nerve dysfunction. They re n objective, quntified nd sensitive indictor for the evlution of sensory functionl disorders nd neurl pthwy integrity. Peer review: Our experimentl findings provide evidence for the cre of ptients undergoing clinicl surgery to minimize the incidence of itrogenic spinl cord injury, indicting tht monitoring of somtosensory evoked potentils cn detect erly 3093

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