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Biomedical subjects

P de Haan

Publications and source records attributed to P de Haan.

At least 19 recordsLinked to original sources
PubMed2006

Inhibition of human immunodeficiency virus type 1 by RNA interference using long-hairpin RNA.

Inhibition of virus replication by means of RNA interference has been reported for several important human pathogens, including human immunodeficiency virus type 1 (HIV-1). RNA interference against these pathogens has been accomplished by introduction of virus-specific synthetic small interfering RNAs (siRNAs) or DNA constructs encoding short-hairpin RNAs (shRNAs). Their use as therapeutic antiviral against HIV-1 is limited, because of the emergence of viral escape mutants. In order to solve this durability problem, we tested DNA constructs encoding virus-specific long-hairpin RNAs (lhRNAs) for their ability to inhibit HIV-1 production. Expression of lhRNAs in mammalian cells may result in the synthesis of many siRNAs targeting different viral sequences, thus providing more potent inhibition and reducing the chance of viral escape. The lhRNA constructs were compared with in vitro diced double-stranded RNA and a DNA construct encoding an effective nef-specific shRNA for their ability to inhibit HIV-1 production in cells. Our results show that DNA constructs encoding virus-specific lhRNAs are capable of inhibiting HIV-1 production in a sequence-specific manner, without inducing the class I interferon genes.

Animals↗
PubMed2001

Spinal cord monitoring: somatosensory- and motor-evoked potentials.

Monitoring myogenic motor EPs after transcranial electrical stimulation is effective in detecting spinal cord ischemia. During thoracoabdominal aortic aneurysm surgery, this technique is sufficiently rapid to allow timely interventions aimed at correcting ischemic conditions and preserving spinal cord blood flow. If strategies are applied to protect the spinal cord during thoracoabdominal aortic aneurysm repair (e.g., distal bypass, cerebrospinal fluid drainage, reattachment of segmental arteries), motor EP monitoring should be included in this protocol to improve neurologic outcome further. Although SSEPs provide information regarding the adequacy of spinal cord blood flow, monitoring SSEPs during thoracoabdominal aortic aneurysm repair has serious limitations. The response time is too slow to be of practical use. SSEPs also do not provide information regarding anterior horn motor function and supply, whereas the motor neurons in the anterior horn are most likely to sustain ischemic injury.

Evoked Potentials, Motor↗
PubMed2001

Pharmacologic neuroprotection in experimental spinal cord ischemia: a systematic review.

Various surgical procedures may cause temporary interruption of spinal cord blood supply and may result in irreversible ischemic injury and neurological deficits. The cascade of events that leads to neuronal death following ischemia may be amenable to pharmacological manipulations that aim to increase the tolerable duration of ischemia. Many agents have been evaluated in experimental spinal cord ischemia (SCI). In order to investigate whether an agent is available that justifies clinical evaluation, the literature on pharmacological neuroprotection in experimental SCI was systematically reviewed to assess the neuroprotective efficacy of the various agents. In addition, the strength of the evidence for neuroprotection was investigated by analyzing the methodology. The authors used a systematic review to conduct this evaluation. The included studies were analyzed for neuroprotection and methodology. In order to be able to compare the various agents for neuroprotective efficacy, relative risks and confidence intervals were calculated from the data in the results sections. A total of 103 studies were included. Seventy-nine different agents were tested. Only 14 of the agents tested did not afford protection at all. A large variation was observed in the experimental models to produce SCI. This variation limited comparison of the individual agents. In 48 studies involving 31 single agents, the relative risks and confidence intervals could be calculated. An analysis of the methodology revealed poor temperature management and lack of statistical power in the majority of the 103 studies. The results suggest that numerous agents may protect the spinal cord from transient ischemia. However, poor temperature management and lack of statistical power severely weakened the evidence. Consequently, clinical evaluation of pharmacological neuroprotection in surgical procedures that carry a risk of ischemic spinal cord damage is not justified on the basis of this study.

Animals↗
PubMed2001

Ischemic transverse myelopathy after endovascular repair of a thoracic aortic aneurysm.

PURPOSE: To report a dramatic complication after endovascular repair of a descending thoracic aortic aneurysm (TAA) and to present a classification system and possible methods to avoid spinal cord ischemia. CASE REPORT: A 48-year-old man with a descending TAA between T5 and T9 was treated with endovascular stent-grafts. Fourteen hours after the operation, the patient developed partial transverse myelopathy at level T10. During emergency conversion to open surgery and implantation of a conventional tube graft, 3 intercostal arteries that had been covered by the stent-graft were revascularized. Postoperatively, the neurological deficit improved, and the patient was able to walk again. Methods to predict and possibly prevent the induction of spinal cord ischemia after endovascular repair of TAA are suggested. CONCLUSIONS: Endovascular repair of TAA may induce spinal cord ischemia; pre- and intraoperative assessment of involved intercostal arteries should be performed.

Aortic Aneurysm, Thoracic↗
PubMed2000

Thermal spin-wave scattering in hot-electron magnetotransport across a spin valve.

The role of thermal scattering in spin-dependent transport of hot electrons at 0.9 eV is studied using a spin-valve transistor with a soft Ni(80)Fe(20)/Au/Co base. Spin-dependent scattering makes the collected electron current depend sensitively on the magnetic state of the base. The magnetocurrent reaches 560% at 100 K, decays with increasing temperature, and a huge effect of 350% still remains at room temperature. The results demonstrate that thermal spin waves produce quasielastic spin-flip scattering of hot electrons, resulting in mixing of the two spin channels.

Journal Article↗
PubMed2000

Epidural versus subdural spinal cord cooling: cerebrospinal fluid temperature and pressure changes.

BACKGROUND: Regional spinal cord cooling can increase the tolerable duration for spinal cord ischemia resulting from aortic clamping. We compared the efficacy of epidural and subdural cooling and the effect of the resulting cerebrospinal fluid-pressure (CSF) increases on spinal cord motor neuron function. METHODS: In 8 pigs, CSF temperature and pressure were assessed in the subdural space at L4, T15, and T7. Saline was infused at 333, 666, and 999 ml/h at four consecutive locations: L4 subdural, L4 epidural, T15 subdural, and T15 epidural. First, the influence of CSF-pressure increases during normothermic infusion on transcranial motor evoked potentials (tc-MEPs) was assessed. Then, hypothermic infusion (4 degrees C) was performed to assess CSF-temperature changes. RESULTS: During normothermic infusion, baseline CSF pressures increased uniformly from 6 +/- 4 mm Hg to 34 +/- 18, 42 +/- 17, and 50 +/- 18 mm Hg with increasing infusion rates (p < 0.001), and did not differ between epidural or subdural infusion. Tc-MEPs indicated spinal cord ischemia in 6 animals when CSF pressures reached 65 +/- 11 mm Hg. During hypothermic infusion, CSF temperatures decreased from 37 degrees to 35 +/- 1.2 degrees, 31 +/- 2.2 degrees, and 28 +/- 2.8 degrees C, but increasing CSF-temperature gradients were observed between the infusion location and distant segments. Subdural cooling resulted in lower CSF temperatures (p < 0.001), but caused larger CSF-pressure increases (p < 0.001). CONCLUSIONS: Subdural and epidural infusion cooling produce localized spinal cord hypothermia in pigs. The concurrent pressure increases, however, are uniformly distributed and can result in tc-MEP evidence of ischemia.

Animals↗
PubMed2000

Effect of ischemic pretreatment on heat shock protein 72, neurologic outcome, and histopathologic outcome in a rabbit model of spinal cord ischemia.

OBJECTIVE: In the present study, we investigated the effect of ischemic pretreatment on heat shock protein 72 concentration and neurologic and histopathologic outcome after transient spinal cord ischemia. METHODS: In 28 New Zealand White rabbits, an aortic occlusion device was placed infrarenally. The animals were randomly assigned to 2 groups: ischemic pretreatment (n = 14 animals) and control (n = 14 animals). The duration of ischemic pretreatment was 6 minutes. After 24 hours, the aorta was occluded for 26 minutes in both groups of animals. Neurologic function was assessed 24 and 48 hours after the definite ischemic insult. At 48 hours, the animals were killed for histopathologic evaluation of the spinal cord. In a separate set of animals, heat shock protein 72 levels were determined in the lumbar spinal cord after both a 6- and 10-minute ischemic period, with the use of a Western blot analysis. RESULTS: No significant difference in neurologic outcome between the groups was observed at 24 and 48 hours. The incidence of paraplegia and severe paresis at 48 hours was 79% in the control group and 92% in the ischemic pretreatment group. There was no difference in histopathologic scores between the groups. Heat shock protein 72 could be clearly detected 1 and 2 days after 6- or 10-minute periods of spinal cord ischemia. CONCLUSIONS: In the present rabbit study, ischemic pretreatment could not induce tolerance against a moderately severe spinal cord ischemic insult, despite increased heat shock protein 72 levels after the preconditioning stimulus.

Animals↗
PubMed2000

Neuroprotective effects of riluzole and ketamine during transient spinal cord ischemia in the rabbit.

BACKGROUND: Massive release of central excitatory neurotransmitters is an important initial step in ischemic neuronal injury, and modification of this process may provide neuroprotection. We studied the protective effects of the voltage-dependent sodium channel antagonist riluzole and the N-methyl-d-aspartate receptor antagonist ketamine on hind limb motor function and histopathologic outcome in an experimental model of spinal cord ischemia. METHODS: Temporary spinal cord ischemia was induced by 29 min of infrarenal balloon occlusion of the aorta in 60 anesthetized New Zealand white rabbits. Animals were randomly assigned to one of four treatment groups (n = 15 each): group C, saline (control); group R, riluzole, 8 mg/kg intravenously; group K, ketamine, 55 mg/kg intravenously; group RK, riluzole and ketamine. After reperfusion, riluzole treatment was continued with intraperitoneal infusions. Normothermia (38 degrees C) was maintained during ischemia, and rectal temperature was assessed before and after intraperitoneal infusions. Neurologic function, according to Tarlov's criteria, was evaluated every 24 h, and infarction volume and the number of eosinophilic neurons and viable motoneurons in the lumbosacral spinal cord was evaluated after 72 h. RESULTS: Neurologic outcome was better in groups R and RK than in groups C and K. All animals in group C (100%) and all animals but one in group K (93%) were paraplegic 72 h after the ischemic insult versus 53% in group R and 67% in group RK (P < 0.01 each). More viable motoneurons were present in groups R and RK than in controls (P < 0.05). CONCLUSIONS: The data indicate that treatment with riluzole can increase the tolerance of spinal cord motoneurons to a period of normothermic ischemia. Intraischemic ketamine did not provide neuroprotection in this model.

Animals↗
PubMed2000

Pharmacologic adjuncts to protect the spinal cord during transient ischemia.

Despite numerous strategies that aim to maintain and restore adequate spinal cord perfusion during thoracoabdominal aortic aneurysm repair, a lower limb neurologic deficit remains a distinct possibility. When critical intercostal arteries originate either at or below the level of repair, transient spinal cord ischemia might occur. Pending on the severity and duration of ischemia, irreversible damage evolves. Therefore, it would be advantageous if adjuncts were available that could enhance neuronal tolerance and improve neuronal survival after episodes of spinal cord ischemia. The beneficial effect of permissive or induced hypothermia is well established. This review focuses on pharmacologic adjuncts. The cascade that leads to neuronal death after ischemia consists of several pathways that act both parallel and sequential. The ischemic cascade provides logical pathogenetic determinants for pharmacologic interventions. Indeed, neuroprotection was attributed to numerous agents in experimental spinal cord ischemia. The clinical use of most of these agents is hampered by their toxicity and side effects. The current status of pharmacologic protection against spinal cord ischemia is summarized, and future directions are provided.

Adjuvants, Pharmaceutic↗
PubMed2000

Assessment of spinal cord ischemia by means of evoked potential monitoring during thoracoabdominal aortic surgery.

Besides renal failure and mesenteric infarction, spinal cord ischemia is the most dreaded complication after thoracoabdominal aortic surgery. Several techniques have been developed to improve neurologic outcome of these massive surgical procedures, including pharmacologic adjuncts, epidural cooling, distal aortic perfusion, cerebrospinal fluid drainage, and reattachment of segmental arteries. The authors developed a technique to assess spinal cord integrity as part of the surgical protocol, dictating operative strategies to restore blood supply to the endangered grey matter. Monitoring motor evoked potentials (MEPs) was performed in experimental studies and in 170 patients with a thoracoabdominal aortic aneurysm. The surgical protocol included left heart bypass and cerebrospinal fluid drainage, and MEP monitoring was applied to identify critical intercostal and lumbar arteries. Based on MEPs, the aggressive surgical approach resulted in a significant reduction of neurologic complications (2.3%).

Animals↗
PubMed1999

Development of spinal cord ischemia after clamping of noncritical segmental arteries in the pig.

BACKGROUND: Blood flow to the thoracolumbar spinal cord is thought to be critically dependent on the arteria radicularis magna. We investigated whether spinal cord blood supply becomes dependent on other, noncritical, segmental arteries if spinal cord perfusion pressure (SCPP) is decreased. The SCPP is equal to the mean arterial pressure (MAP) minus the cerebrospinal fluid (CSF) pressure (SCCP = MAP - CSF). METHODS: The thoracoabdominal aorta was exposed in 10 pigs. Functional integrity of spinal cord motor pathways was assessed with myogenic motor-evoked potentials after transcranial electrical stimulation (tc-MEPs). Using this technique, a group of segmental arteries not critical for spinal cord blood supply was identified. Before, during, and after clamping of the noncritical segmental arteries, spinal cord ischemia was produced by decreasing SCPP by means of increasing CSF pressure, and the SCPP threshold at which tc-MEPs showed evidence of spinal cord ischemia was determined. Ischemic SCPP thresholds, obtained during and after clamping of the noncritical segmental arteries, were compared with the ischemic threshold obtained before clamping (control value). RESULTS: Before noncritical segmental arteries were clamped, ischemic tc-MEP changes occurred when the SCPP was below 15 +/- 5 (SD) mm Hg. With a total of 9 +/- 3 (SD) segmental arteries clamped, the ischemic SCPP threshold was 48 +/- 14 mm Hg (p < 0.01). After the release of all clamps, ischemia occurred at a SCPP of 15 +/- 5 (SD) mm Hg. CONCLUSIONS: In this porcine experiment, clamping of originally noncritical segmental arteries significantly reduced the tolerance of the spinal cord to a decrease in SCPP.

Animals↗
PubMed1999

Strategies to prevent neurologic deficit based on motor-evoked potentials in type I and II thoracoabdominal aortic aneurysm repair.

PURPOSE: Motor-evoked potentials (MEPs) were monitored during thoracoabdominal aortic aneurysm (TAAA) repair to assess spinal cord ischemia and evaluate the subsequent protective strategies to prevent neurologic deficit. METHODS: Between January 1996 and December 1997, 52 consecutive patients with type I (n = 24) and type II (n = 28) TAAA underwent surgery (mean patient age, 60 years; range, 21-78 years). The surgical protocol included left heart bypass, cerebrospinal fluid drainage, and monitoring transcranial myogenic MEPs. When spinal cord ischemia was detected, distal aortic pressure and mean arterial pressure were increased. By means of sequential crossclamping, MEPs were used to identify critical intercostal or lumbar arteries. RESULTS: Reproducible MEPs could be recorded in all patients, and spinal cord ischemia was detected within 2 minutes. During distal aortic perfusion, 14 patients (27%) showed rapid decrease in the amplitude of MEPs to less than 25% of baseline, indicating spinal cord ischemia, which could be corrected by increasing distal aortic pressure. The mean distal aortic pressure to maintain adequate cord perfusion was 66 mm Hg; however, it varied among individuals between 48 and 110 mm Hg. In 24 patients (46%), MEPs disappeared after segmental clamping and returned after reattachment of intercostal arteries. In 9 patients (17%), MEPs disappeared completely, but no intercostal arteries were found. After aortic endarterectomy, 6 or 8 mm Dacron grafts were anastomosed to intercostal arteries, and MEPs returned after reperfusion. Using this aggressive surgical approach based on MEPs, no early or late paraplegia occurred in this series. CONCLUSION: Monitoring of MEPs is an effective technique to assess spinal cord ischemia. Operative strategies based on MEPs prevented neurologic deficits in patients treated for type I and II TAAA.

Adult↗
PubMed1998

Chemokine IP-10 expression in cultured human keratinocytes.

IP-10, a member of the CXC family of chemokines, is considered to play an important role in inflammation via its T-cell chemotactic and adhesion-promoting properties. Elevated IP-10 levels in the epidermis of psoriasis, delayed-type hypersensitivity reactions, cutaneous T-cell lymphoma and fixed drug eruptions prompted us to study its expression in keratinocytes. IP-10 mRNA could be detected using the sensitive RT-PCR method, but not by Northern blotting in RNA preparations from unstimulated normal cultured keratinocytes, indicating a low steady-state level of IP-10 mRNA. Upon stimulation with IFN-gamma, IP-10 mRNA was found to accumulate in high amounts in a time- and dose-dependent manner. Superexpression was found with the combination of IFN-gamma and TNF-alpha or IL-1, although these latter cytokines by themselves did not induce accumulation of IP-10 mRNA. Nuclear run-on experiments performed to investigate the regulation of IP-10 mRNA expression, showed a very high constitutive transcriptional activity of the IP-10 gene in unstimulated keratinocytes, which was not affected by stimulation with IFN-gamma, TNF-alpha, or a combination of IFN-gamma and TNF-alpha. Protein kinase C (PKC) was shown to be involved in IP-10 mRNA expression since the PKC inhibitor H7 decreased IP-10 mRNA accumulation. A protein was isolated from culture supernatants of stimulated keratinocytes using HPLC techniques and, by sequence analysis, was found to be identical to IP-10. The dynamics of secretion of IP-10 protein as monitored by ELISA was shown to parallel the mRNA expression.

Antineoplastic Agents↗
PubMed1998

Reduced renal failure following thoracoabdominal aortic aneurysm repair by selective perfusion.

OBJECTIVES: Renal failure and visceral ischemia are feared complications following thoracoabdominal aortic aneurysm (TAAA) repair, significantly contributing to mortality. This prospective study describes volume- and pressure-controlled perfusion of the renal and visceral arteries during TAAA surgery. METHODS: In 73 consecutive patients (mean age 59 years), TAAA repair (27 type I, 28 type II, 8 type III and 10 type IV) was performed, using retrograde and selective organ perfusion. Sixteen patients had impaired renal function with blood creatinine higher than 100 mmol/l. During the thoracic part of the procedure, the mean distal aortic pressure was kept above 60 mm Hg by means of left-heart bypass. After opening the abdominal aorta, the renal and visceral arteries were individually perfused by means of perfusion catheters (9 French) in the first 33 patients (group I). Volume flow through each catheter was assessed with ultrasound flow meters and maintained at least at 60 ml/min. In addition to volume flow measurements, catheters with pressure sensors were used in the last 40 patients (group II), allowing pressure-controlled selective perfusion. The extent of the aneurysm was comparable in both groups. RESULTS: Mean cross-clamp time for the thoracic part was 46 min, including proximal anastomosis and reattachment of intercostal arteries. Mean cross-clamp time for the abdominal part was 74 min, including re-implantation of intestinal and renal arteries and selective dacron grafts to the celiac-axis arteries (n = 5), superior mesenteric arteries (n = 8) and renal arteries (n = 25), through which the catheters guaranteed continuous perfusion during the time the anastomosis was performed. Urine output was uninterrupted in all patients, irrespective of cross-clamp time. In group I, one patient (3%) developed renal failure and three patients (9%) required temporary peritoneal dialysis. In group II, no patients developed renal failure and two patients (5%) required temporary peritoneal dialysis. Thirteen patients with pre-existing renal impairment did not deteriorate. No patients developed visceral ischemia or multiple-organ failure. Total in-hospital mortality was 6/73 (8%) and was related to cardiopulmonary complications. CONCLUSIONS: Renal and visceral ischemia can be reduced significantly by continuous perfusion during cross-clamping in TAAA repair. Not only sufficient volume flow but also adequate arterial pressure appears to be essential in maintaining renal function.

Aortic Aneurysm, Abdominal↗
PubMed1998

Spinal cord monitoring with myogenic motor evoked potentials: early detection of spinal cord ischemia as an integral part of spinal cord protective strategies during thoracoabdominal aneurysm surgery.

Spinal cord ischemia during resection of thoracoabdominal aortic aneurysms (TAA) can result in lower limb neurological deficits. Spinal cord monitoring can only improve outcome if ischemia is detected before irreversible damage has occurred and protective measures are readily available. Monitorin( spinal cord function with motor evoked potentials (MEPs) is a relatively new technique. With MEP. recorded from the muscle (myogenic MEPs), the vulnerable spinal motoneuronal system is exclusively monitored and ischemia is detected within minutes. Using a strategy aimed at maintaining and restoring spinal cord blood supply (distal aortic perfusion, sequential aortic clamping, and selective segmental artery reattachment), early detection of ischemia allows protective measures to be applied and adjusted immediately, ie, reattaching or safely ligating intercostal arteries, increasing proximal o distal aortic pressures as required, or inducing hypothermia. Recent improvements in the technique fo eliciting myogenic MEPs include multi-pulse stimulation paradigms and the use of a circumferentia cathode. This results in robust and reproducible signals, which are less susceptible to anesthetic interference and allow the use of a constant level of neuromuscular blockade. In conclusion, monitoring myogenic MEPs during a TAA repair has become clinically feasible. The fast detection of spinal cord ischemia allows timely guidance of protective measures.

Animals↗
PubMed1998

Effect of mild hypothermia and the 21-aminosteroid U-74389G on neurologic and histopathologic outcome after transient spinal cord ischemia in the rabbit.

Mild hypothermia and the 21-aminosteroids have both been neuroprotective in several models of cerebral ischemia. In this study we compared the effects of mild hypothermia and the 21-aminosteroid U-74389G, alone and in combination on neurologic and histopathologic outcome after temporary spinal cord ischemia. Forty male anesthetized New Zealand white rabbits were randomized to four groups (n = 10): (a) normothermia (control); (b) U-74389G (3 mg/kg intravenously [i.v.] before aortic occlusion, 1.5 mg/kg i.v. and 10 mg/kg intraperitoneally after occlusion); (c) mild hypothermia (4 degrees C epidural temperature decrease); and (d) mild hypothermia combined with U-74389G. Spinal cord ischemia was produced by 40 min of infrarenal aortic balloon occlusion. Forty-eight hours after the procedure, the neurologic status of the animals was assessed (Tarlov score) and the animals were killed for histologic evaluation. In the normothermic control group, eight of 10 animals became paraplegic. There was a significant reduction of the incidence of paraplegia and overall neurologic deficits and a significant improved Tarlov score in the mild hypothermic group (one animal paraplegic) and in the group with both mild hypothermia and U-74389G (two animals with a mild paraparesis). The histopathologic scores showed significantly less damage in both hypothermic groups. In group 2, U-74389G administration did not improve neurologic or histopathologic outcomes. The results of the current study demonstrate that a slight decrease of intraischemic spinal cord temperature significantly improved neurologic and histopathologic outcomes after experimental spinal cord ischemia. Protection by the 21-aminosteroid at normothermic conditions, or additional protection when U-74389G was added to mild hypothermia, could not be demonstrated.

Anesthesia, Intravenous↗
PubMed1997

Efficacy of transcranial motor-evoked myogenic potentials to detect spinal cord ischemia during operations for thoracoabdominal aneurysms.

OBJECTIVE: Motor-evoked myogenic potentials after transcranial electrical stimulation monitor the vulnerable motoneuronal system of the spinal cord. This study reports our initial experiences with motor-evoked potentials to assess the adequacy of spinal cord perfusion during operations for thoracoabdominal aneurysms. METHODS: In 20 patients undergoing thoracoabdominal aneurysm operations, myogenic motor-evoked potentials were recorded. In 18 patients retrograde aortic perfusion was used. When spinal cord ischemia was detected, distal flow or mean arterial pressure was increased in an attempt to restore cord perfusion. By means of sequential crossclamping, motor-evoked potentials were also used to identify intercostal or lumbar arteries that needed to be reimplanted. RESULTS: Reproducible motor-evoked potentials could be recorded in all patients. During retrograde perfusion, nine patients showed a rapid decrease in the amplitude of motor-evoked potentials to less than 25% of baseline, indicating spinal cord ischemia. In five patients ischemic changes in motor-evoked potentials could be reversed by increasing distal and proximal blood pressures. In four patients ischemic changes during crossclamping necessitated segmental artery reimplantation. In three of these four patients intercostal or lumbar arteries were reattached. In one patient reimplantation of segmental arteries was not possible; this patient awoke paraplegic. Segmental arteries were ligated after confirmation of intact motor-evoked potentials during aortic clamping in eight patients. None of these patients had a neurologic deficit. The absence of motor-evoked potentials at the end of the procedure always indicated a postoperative motor deficit. CONCLUSION: During operations for thoracoabdominal aneurysms, monitoring of motor-evoked potentials is an effective technique to detect spinal cord ischemia within minutes. This modality can be used to guide the management of distal aortic perfusion techniques and may also help to identify segmental arteries that need to be reattached.

Adult↗