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At least 19 recordsLinked to original sources
PubMed1993

Profound systemic hypothermia protects the spinal cord in a primate model of spinal cord ischemia.

Spinal cord ischemia with resultant paraplegia or paraparesis remains an important clinical problem after operations on the thoracoabdominal aorta. Because hypothermia has a protective effect on ischemic neural tissue, we developed a baboon model of spinal cord ischemia to simulate the situation encountered clinically for resection of aneurysms of the thoracoabdominal aorta and to determine whether profound hypothermia produced by hypothermic cardiopulmonary bypass has a protective effect on spinal cord function. After cardiopulmonary bypass was established, the aorta was clamped distal to the left subclavian artery and proximal to the renal arteries for 60 minutes. Group I animals (n = 9) underwent aortic clamping at normothermia (37 degrees C), and group II animals (n = 9) were cooled to a rectal temperature of 15 degrees C before aortic clamping and underwent cardiopulmonary bypass at this temperature until the aorta was unclamped. Of the eight operative survivors in group I, six animals were paraplegic and two were paraparetic, whereas all six group II animals that survived the procedure were neurologically intact (p = 0.0002). The protective effect of hypothermia was associated with blunting of the hyperemic response of spinal cord blood flow (determined by the radioactive microsphere technique) in the lower thoracic and the lumbar segments of the spinal cord after unclamping of the aorta. Profound hypothermia produced by hypothermic cardiopulmonary bypass may be an effective method of protection of the spinal cord in patients undergoing repair of aneurysms of the thoracoabdominal aorta and may reduce the prevalence of ischemic injury to the spinal cord.

Animals↗
PubMed1988

Fluosol and experimental spinal cord ischemia.

Spinal cord ischemia was produced by temporary aortic occlusion for 12.5 min in 27 rabbits. Animals were divided into three groups: Group A received Fluosol DA 20% and 100% oxygen; Group B Fluosol and room air only, and Group C Dextran 40 and 100% oxygen. There was no difference in neurological outcome or in the extent and severity of histologically documented infarction of the spinal cord in the three groups. There was also no difference between these groups and untreated controls previously studied by us.

Animals↗
PubMed2004

Spinal cord blood flow after ischemic preconditioning in a rat model of spinal cord ischemia.

Spinal cord blood flow after ischemic preconditioning is poorly characterized. This study is designed to evaluate spinal cord blood flow patterns in animals after acute ischemic preconditioning. Experiment 1: After a laminectomy and placement of a laser Doppler probe over the lumbar spinal cord to measure spinal cord blood flow, 16 male Sprague-Dawley rats were randomized into two groups: ischemic preconditioning (IPC, n = 8), and control (CTRL, n = 8). Rats in the CTRL and the IPC groups were subjected to 12 min of ischemia directly followed by 60 min of reperfusion. IPC rats received 3 min of IPC and 30 min of reperfusion prior to the 12-min insult period. Experiment 2: After instrumentation, the rats were randomized into three groups: control (CTRL, n = 7), ischemic preconditioning (IPC, n = 7), and time control (TC, n = 4). Rats in the CTRL and the IPC groups were subjected to the same ischemia and reperfusion protocol as above. The TC group was anesthetized for the same time period as the CTRL and the IPC groups, but had no ischemic intervention. Microspheres were injected at baseline and at 15 and 60 min into the final reperfusion. All rats were euthanized and tissue harvested for spinal cord blood flow analysis. In Experiment 1, there was a slight, significant difference in spinal cord blood flow during the ischemic period; however, this difference soon disappeared during reperfusion. In experiment 2, there was no difference in blood flow at any experimental time. The results of these experiments demonstrate that IPC slightly enhances blood flow to the spinal cord during ischemia; however, this effect is not sustained during the reperfusion period.

Animals↗
PubMed1989

Paraplegia caused by local spinal cord ischemia. An animal spinal cord ischemia model.

Local spinal cord ischemia model was established in 11 adult dogs. The anterior spinal artery, posterior spinal artery and radicular artery were cauterized with bipolar cautery. Ischemia of this segment of spinal cord was thus produced followed by paraplegia. The pathological findings of this spinal cord segment were softening and necrosis. The establishment of this animal model of segmental spinal cord ischemia is beneficial to scientific research in basic medicine and clinical practice.

Animals↗
PubMed2005

Emergency endovascular treatment for ruptured abdominal aortic aneurysm and the risk of spinal cord ischemia.

BACKGROUND: Spinal cord ischemia is a rare complication after open surgical repair for ruptured abdominal aortic aneurysms (rAAA). The use of emergency endovascular aortic aneurysm repair (eEVAR) is increasing, and paraplegia has been observed in a few patients. The objective of this study was to assess the incidence and pathogenesis of spinal cord ischemia after eEVAR in greater detail. METHODS: This was a retrospective analysis of patients who had eEVAR for rAAA in three hospitals in The Netherlands and Belgium during a 3-year study period that ended in February 2004. The use of aortouniiliac devices combined with a femorofemoral crossover bypass was the preferred technique. Patients with postoperative symptoms of spinal cord ischemia were identified and the influence of potential risk factors was assessed. These factors included the presence of common iliac artery aneurysms necessitating device limb extension to the external iliac artery with associated overlapping the hypogastric artery, the prolonged interruption of bilateral hypogastric artery arterial inflow during the procedure (defined "functional aortic occlusion time" >30 minutes), and the occurrence of preoperative hemodynamic shock. RESULTS: Thirty-five patients were treated by EVAR and they constituted the study group. The first-month mortality in the study group with EVAR was 23%. Four patients (11.5%) with EVAR developed paraplegia postoperatively; the unilateral or bilateral hypogastric artery in all four patients became occluded during the procedure. In the other 31 patients who did not have paraplegia, the unilateral or bilateral hypogastric arteries became occluded in 14 patients (45%). This constituted a significant difference in the prevalence of hypogastric artery occlusion in patients with or without paraplegia (P = .04). The functional aortic occlusion time was prolonged in all four patients with paraplegia and in five without spinal cord ischemia (P = .0003). All four patients with spinal cord ischemia presented with hemodynamic shock. This factor did not reach a significant difference from nonparaplegic patients. CONCLUSION: Emergency EVAR continues to be a promising approach to reduce the high mortality of rAAA, but the incidence of spinal cord ischemia after endovascular treatment of rAAA was worrisome. Although the pathogenesis is most likely multifactorial, interruption of the hypogastric artery inflow appeared to have significant influence. In patients with aneurysmatic common iliac arteries, any effort should be made to minimize hypogastric occlusion time during the procedure and to maintain hypogastric artery inflow afterwards, either by the use of a bell-bottom iliac extension or by electing open repair.

Aged↗
PubMed2006

Endovascular thoracic aortic repair and previous or concomitant abdominal aortic repair: is the increased risk of spinal cord ischemia real?

Spinal cord ischemia after endovascular thoracic aortic repair remains a significant risk. Previous or concomitant abdominal aortic repair may increase this risk. This investigation reviews the occurrence of spinal cord ischemia after endovascular repair of the descending thoracic aorta in patients with previous or concomitant abdominal aortic repair. Over an 8-year period, 125 patients underwent endovascular exclusion of the thoracic aorta at the Mount Sinai Medical Center. Twenty-eight of these patients had previous or concomitant abdominal aortic repair. The 27 patients who underwent staged repairs all had cerebrospinal fluid (CSF) drainage during and following repair. This population was analyzed for the complication of spinal cord ischemia and factors related to its occurrence. Mean follow-up was 19.3 months (range 1-61). Spinal cord ischemia developed in four of the 28 patients (14.3%) who underwent endovascular thoracic aortic repair with previous or concomitant abdominal aortic repair, while one of 97 patients (1.0%) developed ischemia among the remaining thoracic endograft population. One patient with concomitant abdominal aortic repair developed cord ischemia that manifested 12 hr following the procedure. The remaining three patients with previous abdominal aortic repair developed more delayed-onset paralysis ranging from the third postoperative day to 7 weeks following repair. Irreversible cord ischemia occurred in three patients, with full recovery in one patient. Major complications from CSF drainage occurred in one patient (3.7%). Spinal cord ischemia occurred at a markedly higher rate in patients with previous or concomitant abdominal aortic repair. This risk continued beyond the immediate postoperative period. The benefit of perioperative and salvage CSF drainage remains to be determined.

Angioplasty↗
PubMed2006

Diffusion-weighted MR imaging (DWI) in spinal cord ischemia.

INTRODUCTION: Spinal cord infarction is a rare clinical diagnosis characterized by a sudden onset of paralysis, bowel and bladder dysfunction, and loss of pain and temperature perception, with preservation of proprioception and vibration sense. Magnetic resonance imaging (MRI) usually demonstrates intramedullary hyperintensity on T2-weighted MR images with cord enlargement. However, in approximately 45% of patients, MR shows no abnormality. Diffusion-weighted MR imaging (DWI) has been widely used for the evaluation of a variety of brain disorders, especially for acute stroke. Preliminary data suggest that DWI has the potential to be useful in the early detection of spinal infarction. METHODS: We performed DWI, using navigated, interleaved, multishot echo planar imaging (IEPI), in a series of six patients with a clinical suspicion of acute spinal cord ischemia. RESULTS: In all patients, high signal was observed on isotropic DWI images with low ADC values (0.23 and 0.86x10(-3) cm(2)/s), indicative of restricted diffusion. CONCLUSION: We analyzed the imaging findings from conventional MR sequences and diffusion-weighted MR sequences in six patients with spinal cord infarction, compared the findings with those in published series, and discuss the value of DWI in spinal cord ischemia based on current experience. Although the number of patients with described DWI findings totals only 23, the results of previously published studies and those of our study suggest that DWI has the potential to be a useful and feasible technique for the detection of spinal infarction.

Adolescent↗
PubMed1993

Inactivation and subcellular redistribution of Ca2+/calmodulin-dependent protein kinase II following spinal cord ischemia.

Reversible spinal cord ischemia in rabbits induced a rapid loss of Ca2+/calmodulin-dependent protein kinase II (CaM kinase II) activity measured as incorporation of phosphate into exogenous substrates. About 70% of the activity was lost from the cytosolic fraction of spinal cord homogenates after 15 min of ischemia preceding irreversible paraplegia, which takes 25 min in this model. The loss of enzyme activity correlated with a loss of in situ renaturable autophosphorylation activity and a loss of CaM kinase II alpha and beta subunits in the cytosol detected by immunoblotting. CaM kinase II activity in the particulate fraction also decreased but the protein levels of the alpha and beta subunits increased. Thus ischemia resulted in an inactivation of CaM kinase II and a sequential or concurrent subcellular redistribution of the enzyme. However, denaturation and renaturation in situ of the CaM kinase subunits immobilized on membranes partly reversed the apparent inactivation of the enzyme in the particulate fraction. CaM kinase II activity was restored after reperfusion following short (< or = 25 min) durations of ischemia but not after longer durations (60 min) that result in irreversible paraplegia. The ischemia-induced inactivation of CaM kinase II, which phosphorylates proteins regulating many cellular processes, may be important in the cascade of events leading to delayed neuronal cell death.

Animals↗
PubMed2006

Effects of cyclosporin a on neurological outcome and serum biomarkers in the same setting of spinal cord ischemia model.

Spinal cord ischemic injury is one of the feared complications during aortic cross-clamping. The aim of this study was to investigate whether cyclosporin A (CsA) has a protective effect on spinal cord during ischemia in a rabbit model. A total of 22 New Zealand white rabbits were studied in three groups. One of the groups served as a sham group (n=7), in which only laparatomy was performed and closed. One group served as a control group (n=7), in which rabbits had their abdominal aortas cross-clamped for 40 min following median laparatomy. The last group was the CsA group (n=8), in which rabbits underwent the same procedure as the control group as well as CsA infusion at 20 mg/(kg . hr) over 60 min starting with aortic cross-clamping and continuing in the first 20 min of reperfusion. Neurological outcome of rabbits was evaluated according to Johnson's scale at postoperative hours 24 and 48 in all groups, and then they were killed. Their spinal cords were harvested, and segments corresponding to L4-L6 were prepared for pathological examination. Serum neuron-specific enolase (NSE) and nitric oxide (NO) levels were measured prior to and following aortic occlusion, and comparisons were made. Physiological data were similar in all groups. Rabbits in the sham group did not have any neurological deficit. However, all rabbits in the control group showed severe neurological deficits, including total paraplegia in five. According to Johnson's scale, neurological status of the rabbits at postoperative hour 48 was better in the CsA group compared to controls (p<0.01). Pathological examination of spinal cord specimens revealed a higher viability index in the CsA group compared to controls (p<0.01). Serum NSE and NO levels were lower in CsA-treated animals compared to controls. Our results demonstrate that CsA, when administered during ischemia and in the early period of reperfusion, may reduce neuronal damage in the spinal cord in a rabbit model of transient spinal cord ischemia.

Animals↗
PubMedDate not supplied

Prevention of spinal cord ischemia by monitoring spinal cord perfusion pressure and somatosensory evoked potentials.

The pressure difference between mean distal aortic pressure (MDAP) and cerebrospinal fluid pressure (CSFP), defined as relative spinal cord perfusion pressure (SCPP), and somatosensory evoked potentials (SEP) were monitored intraoperatively to detect and prevent intraoperative ischemic spinal cord injury in 19 patients who required cross-clamping of the descending thoracic aorta. Temporary axillo-femoral shunt utilizing a 10 mm woven Dacron tube graft was employed in 10 patients and partial cardiopulmonary bypass in nine. Ischemic SEP changes were seen in five patients. Two patients, whose SCPPs were 32 and 35 mmHg, experienced the complete loss of SEP and developed paraplegia. In the other three cases, increase of MDAP and/or withdrawal of cerebrospinal fluid (CSF) were performed to increase the SCPP to more than 40 mmHg when ischemic SEP changes occurred. SEP gradually recovered in two cases. The other patient underwent reimplantation of intercostal arteries since the ischemic SEP changes did not revert. These three patients recovered without any neurological deficit. In the other 14 cases without ischemic SEP changes, SCPP was kept at more than 40 mmHg during aortic cross-clamping. We conclude that the maintenance of SCPP at more than 40 mmHg by increasing MDAP and/or withdrawing CSF is an effective procedure in preventing postoperative paraplegia.

Adult↗
PubMed2005

Calbindin D-28k is expressed in the microvascular basal lamina in the ventral horn at early time after transient spinal cord ischemia in the rabbit.

Much evidence has been accumulated that the increased expression of calbindin D-28k (CB) is involved in the blockade of calcium-evoked excitotoxicity in cerebral ischemia. We investigated the expression of CB in the basal lamina of microvessels in the ventral horn of the rabbit spinal cord after transient spinal cord ischemia. Spinal cord sections at the level of L7 were immunostained using monoclonal antibody raised against CB at light and electron microscopic levels. CB immunoreactivity was detected in the basal lamina of microvessels at 30 min after ischemic insult. By 3 h after ischemia, CB immunoreactivity was increased in the basal lamina of the microvessels. CB immunoreactivity began to decrease at 6 h after ischemia and nearly disappeared at 48 h after ischemic insult. For calcium detection in the blood vessels of spinal cord, we conducted an alizarin red staining. Alizarin red reactivity was detected in some microvessels at 3 h after ischemic insult. Our results suggest that the ectopic expression of CB in the microvascular basal laminae may be associated with the buffering of calcium in the endothelial cells of microvessels after ischemic damage.

Animals↗
PubMed1993

Effects of spinal cord ischemia on evoked potential recovery and postischemic regional spinal cord blood flow.

The effects of spinal cord ischemia on spinal cord blood flow (SCBF) and somatosensory (SSEP) and motor (MEP) evoked potentials were investigated in a rabbit model of reversible spinal cord ischemia. Spinal cord ischemia was produced by balloon occlusion of the infrarenal aorta for 30, 60, and 90 min. SCBF, SSEPs, and MEPs were measured before, during, and 1 h after aortic occlusion. Aortic occlusion produced absolute ischemia of the caudal cord followed by hyperemia upon reperfusion. SSEP's and MEP's were obliterated during ischemia but demonstrated gradual albeit incomplete recovery following reperfusion with amplitude recovery inversely proportional to the duration of ischemia. Later peaks were more severely affected by a given period of ischemia than were early waves. In general, SSEP's were more resistant to ischemia than were MEP's although the differences were not significant.

Animals↗
PubMed2002

Inter-relationships between spinal cord blood flow, neuronal death and neurological function in rabbit spinal cord ischemia.

Following rabbit spinal cord ischemia we measured histology, neurological outcome and spinal cord blood flow to investigate relationships between these quantities over a range of ischemia durations. Rabbits underwent reversible spinal cord ischemia induced by temporary aortic artery occlusion for zero to 65 min. In one cohort, surviving spinal cord cells were counted after 4 days of reperfusion using computer image analysis (n=23). Neurological outcome (paraplegic or non-paraplegic) was assessed in another group (n=381) after 18 h of reperfusion. A third group (n=8) had spinal cord blood flow measured by radioactive tracer immediately after ischemia. Histological analysis showed fewer motor neurons and astrocytes surviving as ischemia duration increased. Following 13 min (95% confidence interval (CI), 6 to 27) of ischemia 50% of low lumbar cord motor neurons remained alive; 50% of rabbits were paraplegic following 28.4 (26.7 to 30.0) min of ischemia; 28% (17% to 48%) of low lumbar motor neurons survived at this duration; 5% of rabbits were permanently paraplegic following 13.6 (10.6 to 16.1) min of ischemia, although only 52% (30% to 87%) of lower spinal cord motor neurons survived. Low lumbar cord blood flow was reduced to 2% of flow in non-ischemic thoracic cord after 25 and 60 min of ischemia (0.52 and 0.59 ml/100 g/min, respectively). These data support a fundamental hypothesis on which experimental ischemia is based: that substantial neuronal death follows directly from reversible ischemia and leads to permanent neurological deficit.

Animals↗
PubMed2006

Transcranial motor-evoked potentials monitoring can detect spinal cord ischemia more rapidly than spinal cord-evoked potentials monitoring during aortic occlusion in rats.

In this study, we evaluated the efficacy of transcranial motor-evoked potentials (tc-MEPs), compared with segmental spinal cord-evoked potentials (SCEPs), for detecting spinal cord ischemia (SCI) and assessed the relationship between neurological outcome and tc-MEPs or SCEPs in the rat aortic occlusion model. In the rats, SCI was induced by aortic occlusion for 10 min with a balloon catheter. At first, tc-MEPs (Group A: n = 6) or segmental SCEPs (Group B: n = 6) was recorded during SCI. Second, in using the quantal bioassay for the relationship between an interval of aortic occlusion and the probability of positive response in tc-MEPs or segmental SCEPs, the P50(MEP) and P50(SCEP) which represent the interval of aortic occlusion associated with 50% probability of assessment of ischemic spinal cord dysfunction by tc-MEP and SCEP were analyzed. The amplitude of tc-MEPs decreased significantly at 30 s and disappeared completely at 2 min after aortic occlusion. In Group B, it took about 6 min after aortic occlusion to diminish SCEP signal amplitude by approximately 50%. P50(MEP) obtained in the quantal analysis was 0.3 +/- 0.1 min. P50(SCEP) was calculated as 6.2 +/- 0.5 min that was significantly (P < 0.01) longer than P50(MEP). Our data indicated that tc-MEP monitoring could detect the onset of SCI so rapidly in comparison with segmental SCEP monitoring, which could provide therapeutic windows in a surgical approach that includes spinal cord protection.

Animals↗
PubMed1994

Monitoring for spinal cord ischemia by use of the evoked spinal cord potentials during aortic aneurysm surgery.

PURPOSE: This clinical study was to evaluate changes of evoked spinal cord potentials (ESCPs) elicited by direct spinal cord stimulation and to determine their relation to spinal cord ischemia during aortic aneurysm surgery. METHODS: We monitored descending ESCPs from the thoracic spinal cord and lumbar enlargement after cervical spinal cord stimulation (thoracic descending ESCP and lumbar descending ESCP), and segmental ESCP at lumbar enlargement elicited by bilateral tibial nerve stimulation in 22 aortic aneurysm surgical operations. RESULTS: ESCP changes were classified into three types: (1) decrease of amplitude in lumbar descending ESCP and segmental ESCP; (2) decrease of amplitude in segmental ESCP alone; (3) decrease of amplitude in all ESCPs. The late negative waves of both lumbar descending ESCP and segmental ESCP were more sensitive than other components of ESCPs. Postoperative paraplegia occurred in the two cases that showed persistent diminution of amplitude in the late negative waves. Segmental ESCP was less reliable than lumbar descending ESCP, because it depended entirely on the adequate perfusion of the lower extremities. CONCLUSIONS: Lumbar descending ESCP was the best method for the spinal cord ischemia during aortic aneurysm surgery. Spinal cord ischemia could be detected by diminution in the amplitude of the late negative wave of lumbar descending ESCP. The recovery amplitude of the late negative wave after declamping correlated with the neurologic outcome.

Aged↗
PubMed1995

Mild hypothermia protects against irreversible damage during prolonged spinal cord ischemia.

Mild hypothermia to 32 degrees C protected the spinal cords of 5 rabbits subjected to 90 min of surgically created spinal cord ischemia. Spinal cord ischemia was produced in 10 New Zealand White rabbits by transection of four out of the five segmental arteries arising from the abdominal aorta below the renal arteries plus 90-min occlusion of the remaining segmental artery 24 hr later. Of these 10 rabbits, 5 served as controls. Recovery, or failure to recover, as assessed by examining the rabbits for permanent loss of sensory and motor function in the hind limbs, was compared in the two groups. The duration of the ischemia was sufficient to lead to a total or near total loss of sensory and motor function in all control rabbits. These results may have implications for the care of patients subjected to spinal cord ischemia.

Animals↗
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↗
PubMed2003

Linolenic acid prevents neuronal cell death and paraplegia after transient spinal cord ischemia in rats.

PURPOSE: Spinal cord ischemia is a devastating complication of thoracic and thoracoabdominal aortic surgery. Recent studies have suggested a neuroprotective effect of polyunsaturated fatty acids against cerebral ischemia. We investigated the effect of linolenic acid (LIN) in a rat model of spinal cord ischemia. METHODS: Rats were subjected to cross-clamping of the aortic arch and left subclavian artery for 14 minutes. Groups were as follows: sham operation (n = 15); ischemia (n = 15), receiving only vehicle; LIN A (n = 15), receiving LIN before clamping; and LIN B (n = 15), receiving LIN at onset of reperfusion. Neurologic status was assessed daily for 7 days. Spinal cords were harvested for histopathologic analysis, TUNEL staining, and immunohistochemistry for Bax, heat shock protein 70 (HSP70), and nuclear factor-kappaB. RESULTS: Ischemic rats had severe and definitive paraplegia. LIN-treated rats had significantly better neurologic function. Histopathologic analysis disclosed severe neuronal necrosis in the lumbar gray matter of ischemic rats, whereas most of the LIN-treated rats sustained mild to moderate injury. LIN reduced the loss of motor neurons at 7 days (LIN A, 17 +/- 6, and LIN B, 15 +/- 7, versus ischemia, 6 +/- 2 per section; P <.05). LIN prevented apoptotic neuronal cell death, Bax immunoreactivity of the pro-apoptotic protein Bax, and the nuclear transcription factor NF-kappaB. Nuclear HSP70 immunoreactivity was noted exclusively in motor neurons from LIN-treated rats and not in motor neurons from ischemic rats. CONCLUSION: These results suggest that LIN can induce protection against ischemia in the spinal cord, thereby preventing both necrosis and apoptosis of motor neurons.

Analysis of Variance↗