Abstract
Objective:
Prehospital neuroprotectant therapy in combination with thrombolysis is a potential treatment strategy in acute ischemic stroke allowing for earlier therapy start and bridging period until in-hospital therapies. We describe prehospital administration of magnesium sulfate (Mg) vs. placebo for neuroprotection followed by post-arrival thrombolysis (TPA).
Methods:
We analyzed subjects who received TPA in the NIH Field Administration of Stroke Therapy Magnesium (FAST-MAG) clinical trial, a phase 3 randomized clinical trial of patients presenting within 2 h of last known well time (LKWT). Primary outcome was disability measured on the modified Rankin Scale (mRS) at 90 days.
Results:
Among identified 401 cases, 214 received Mg and 187 received placebo followed by TPA. Mean (±SD) age was 70±13 years, 46% women, and median Los Angeles Motor Scale (LAMS) was 4 (IQR 3-5). Median LKWT to prehospital initiation time was 46 min (IQR 35-65), and 150 min (IQR 124-171) to thrombolysis. The median prehospital study infusion exposure prior to thrombolysis start was 93 (IQR 75-117) min. In patients with NIHSS >15, the Mg group had a higher proportion achieving favorable 90-day outcomes (mRS 0–2) and lower median LAMS scores compared with placebo, although these findings were not supported by overall 90-day outcomes mRS analysis and should be considered hypothesis-generating.
Conclusions:
Prehospital magnesium followed by alteplase was feasible and safe but did not demonstrate a significant overall clinical benefit. The main contribution of this analysis is to quantify the substantial prereperfusion exposure interval achievable with prehospital neuroprotective therapy, supporting this model for future agents requiring early biological exposure before reperfusion.
Keywords: Neuroprotection, Magnesium, Thrombolysis, Ischemic stroke
Introduction
Stroke is the second leading cause of death worldwide.1 Reperfusion therapies for the treatment of acute ischemic stroke (AIS) including intravenous thrombolytics like tissue plasminogen activator (TPA) and endovascular mechanical thrombectomy are effective in reducing disability.2,3 Despite the efficacy of reperfusion therapy, clinical efficacy is limited by the need for neuroimaging before treatment decision and resulting delays in treatment initiation.3,4 Many stroke patients are disabled despite receiving these treatments. This highlights the unmet need for bridging neuroprotection (NP) while patients await reperfusion and revascularization treatment initiation. While awaiting reperfusion, bridging NP agents that freeze or slow infarct progression offer an opportunity to preserve penumbral tissue via attenuation of the ischemic cascade in neurons.5,6 There have been numerous trials aimed at identifying viable NP therapies; however, none have been shown to provide any definitive clinically significant benefit. Several reviews suggest prolonged time to treatment initiation was a constraint upon the effectiveness of NP in these trials,7,8 and earlier initiation to preserve penumbral tissue may be a critical element for success in future studies.4
Magnesium sulfate has been investigated as a potential neuroprotective agent in acute ischemic stroke due to its multiple complementary mechanisms of action. In preclinical models, magnesium exerts vasodilatory effects on cerebral vasculature, which may enhance collateral blood flow to ischemic regions.9 In addition, it has several direct neuroprotective properties, including antagonism of N-methyl--D-aspartate (NMDA) receptors, thereby reducing excitotoxic calcium influx, as well as modulation of voltage-gated calcium channels.10,11 Magnesium has also been shown to stabilize cellular membranes, attenuate oxidative stress, and reduce inflammatory responses in ischemic tissue.12 Collectively, these effects may limit neuronal injury and preserve tissue viability within the ischemic penumbra, providing a strong biological rationale for its evaluation as an early neuroprotective intervention in stroke.12
The Field Administration of Stroke Therapy– Magnesium (FAST-MAG) was the first pivotal phase 3, multicenter, randomized, double-blind, placebo-controlled clinical trial to successfully coordinate delivery of a potential NP agent in the prehospital setting.13 The primary hypothesis was that prehospital initiation of Mg in patients with a suspected stroke would reduce the severity of disability at 90 days. Between January 2005 and December 2012, a total of 1700 patients underwent randomization and received either an infusion of Mg or placebo. We describe a subset of patients enrolled in the FAST-MAG trial that received the study-drug in the prehospital setting, followed by TPA in the hospital. We aim to quantify the duration of NP exposure prior to TPA, a metric that was not directly reported in the original trial, as well as describe the functional outcomes in this group.
Methods
We used the STROBE checklist for cross-sectional studies for this manuscript reporting. Details of the original FAST-MAG phase 3 trial methods and patient selection have been published previously.13,14 To better characterize outcomes of patients who received the NP study drug in combination with TPA (Alteplase), we used the FAST-MAG trial database to identify all enrolled patients who had received TPA upon hospital arrival after field NP agent start.
The FAST-MAG study randomly assigned patients in a 1:1 ratio to either receive initiation of magnesium or placebo infusion in the prehospital setting to all patients with suspected stroke within two hours of last known well. Patients in the magnesium-treatment group received an initial 4 g bolus of magnesium sulfate administered over 15 min (54 mL normal saline), followed by a continuous infusion of 16 g magnesium in 240 mL of 0.9% normal saline at 10 mL/h for 24 h.13 Serum magnesium levels were measured separately by a single dedicated unblinded observer after study enrollment to preserve blinding of treatment allocation for all other study personnel and investigators.15 IV TPA was administered to all patients who met treatment criteria of the national practice guidelines from the American Stroke Association during the study time-period.16
To quantify the duration of NP exposure as a potential modifier of TPA effect, the primary descriptive outcome of interest was the time from Mg vs placebo initiation to the administration of TPA. In line with the original FAST-MAG trial, the primary clinical efficacy outcome of interest was reported as the degree of disability after 3 months. This functional outcome was assessed using the modified Rankin scale (mRS). Secondary clinical efficacy outcomes were analyzed at 4 days and 3 months, including LAMS, GCS, NIHSS, and Barthel index. Safety events were also assessed in both groups, including transformation to any radiologic intracranial hemorrhage and overall mortality (Table 3). All outcomes were analyzed by three brackets of NIHSS at Hospital Arrival: NIHSS ≤8 (mild to moderate), 9–15 (moderate), and >15 (severe).
Table 3.
Efficacy and safety outcomes at 3 months.
| Outcomes | NIHSS at Hopsital Arrival ≤8 |
NIHSS at Hopsital Arrival 9-15 |
NIHSS at Hopsital Arrival > 15 |
||||||
|---|---|---|---|---|---|---|---|---|---|
| TPA + Pl (n = 65) |
TPA + Mg (n = 81) |
P-value | TPA + Pl (n = 51) |
TPA + Mg (n = 58) |
P-value | TPA + Pl (n = 71) |
TPA + Mg (n = 75) |
P-value | |
| Day 4 Outcomes | |||||||||
| mRS, Median (IQR) | 3.5 (1-4) | 2.5 (1-4) | 0.93 | 4.0 (3-4) | 4.0 (3-5) | 0.73 | 5.0 (4-5) | 5.0 (4-5) | 0.46 |
| LAMS | |||||||||
| Median (IQR) | 2.0 (0-4) | 1.0 (0-5) | 0.53 | 3.0 (1-5) | 3.0 (1-5) | 0.25 | 5.0 (3-5) | 5.0 (3-5) | 0.72 |
| Mean (SD) | 2.1 (1.9) | 1.9 (2.0) | 0.81 | 3.3 (1.9) | 2.8 (2.0) | 0.37 | 4.1 (1.8) | 4.0 (1.9) | 0.77 |
| GCS | |||||||||
| Median (IQR) | 15.0 (15-15) | 15.0 (15-15) | 0.02 | 15.0 (15-15) | 15.0 (15-15) | 0.27 | 15.0 (11-15) | 15.0 (11-15) | 0.90 |
| Mean (SD) | 14.1 (2.4) | 15.0 (0.3) | <0.001 | 13.4 (3.5) | 14.4 (1.8) | <0.001 | 11.5 (4.4) | 11.4 (4.3) | 0.83 |
| NIHSS, mean (SD) | 5.7 (8.4) | 4.1 (4.7) | 0.04 | 10.5 (11.0) | 7.7 (7.4) | 0.09 | 18.1 (11.8) | 18.3 (12.3) | 0.60 |
| Barthel, mean (SD) | 73.8 (33.5) | 75.6 (32.3) | 0.88 | 45.5 (38.5) | 51.6 (36.2) | 0.45 | 14.0 (23.7) | 24.6 (34.3) | <0.001 |
| Symptomatic ICH, n (%) | 9 (13.8) | 6 (7.4) | 0.20 | 1 (2.0) | 5 (8.6) | 0.13 | 4 (5.6) | 2 (2.7) | 0.51 |
| Day 90 Outcomes | |||||||||
| mRS, Median (IQR) | 2.0 (1-3) | 2.0 (1-3) | 0.76 | 2.0 (1-4) | 3.0 (2-3) | 0.88 | 4.0 (3-5) | 5.0 (2-5) | 0.45 |
| mRS 90d 0-1, n (%) | 29 (44.6) | 43 (53.1) | 0.35 | 18 (35.3) | 18 (31.0) | 0.58 | 5 (7.0) | 11 (14.7) | 0.15 |
| mRS 90d 0-2, n (%) | 46 (70.8) | 62 (76.5) | 0.52 | 28 (54.9) | 28 (48.3) | 0.42 | 10 (14.1) | 21 (28.0) | 0.04 |
| LAMS | |||||||||
| Median (IQR) | 0.0 (0-2) | 0.0 (0-2) | 0.93 | 1.5 (0-3) | 1.0 (0-3) | 0.39 | 4.0 (1-5) | 3.0 (1-5) | 0.04 |
| Mean (SD) | 0.8 (1.4) | 0.8 (1.4) | 0.84 | 1.5 (1.5) | 1.3 (1.6) | 0.76 | 3.3 (2.0) | 2.5 (2.1) | 0.45 |
| NIHSS, mean (SD) | 3.1 (8.2) | 2.5 (6.9) | 0.42 | 9.8 (15.6) | 7.1 (13.1) | 0.14 | 18.1 (16.2) | 19.0 (17.7) | 0.10 |
| Mortality 90d, n (%) | 2 (3.1) | 2 (2.5) | 0.82 | 8 (15.7) | 6 (10.3) | 0.41 | 17 (23.9) | 25 (33.3) | 0.21 |
Statistical analysis
For normally distributed continuous variables pairwise comparisons were performed with Student’s t-test. Results were reported as mean and standard deviation (SD). For dichotomous comparisons the Chi-square test was used. Results were reported as frequency (n) and percentage values. Skewed continuous variables comparisons were performed with the Mann-Whitney U-test. Results were reported as median and inter-quartile range (IQR). P values ≤0.05 were considered significant. Statistical analyses were performed using SPSS version 30.
Results
A total of 1700 patients were enrolled in FAST-MAG between January 2005 and December 2012. Of these, 401 patients were identified to have an ischemic stroke and received intravenous thrombolysis with TPA, with exclusion of any mechanical thrombectomy procedures. Among them, 214 were assigned to the Mg group and 187 assigned to the placebo group. Demographic and clinical characteristics were similar between the two study groups (shown in Table 1). Among 401 patients included in this study, mean age was 70 (SD ±13.5) years, and 46% were women. The median pretreatment Los Angeles Motor Scale (LAMS) was 4 (IQR 3-5) and GCS score was 15 (IQR 12-15). Mean serum magnesium levels were significantly higher in the magnesium group compared with placebo (3.6 ± 1.1 vs 1.9 ± 0.37, p < 0.001), supporting effective systemic delivery of the neuroprotectant intervention (Table 1).
Table 1.
Characteristics of patients at baseline.
| Characteristics | TPA + Pl (n = 187) |
TPA + Mg (n = 214) |
P-value |
|---|---|---|---|
| Age (Mean, SD) | 69.9 (13.9) | 70.6 (13.2) | 0.49 |
| Sex Female (N, Percent) | 94 (50.3) | 92 (43.0) | 0.15 |
| Race, n (%) | |||
| White | 140 (74.9) | 162 (75.7) | 0.48 |
| Black/African American | 30 (16.0) | 27 (12.6) | |
| Asian | 17 (9.1) | 25 (11.7) | |
| Ethnicity – Hispanic, n (%) | 41 (21.9) | 42 (19.6) | 0.57 |
| Medical History | |||
| Hypertension, n (%) | 143 (76.5) | 168 (78.5) | 0.62 |
| Diabetes, n (%) | 50 (26.7) | 42 (19.6) | 0.09 |
| Hyperlipidemia, n (%) | 94 (50.3) | 114 (53.3) | 0.55 |
| Atrial fibrillation, n (%) | 38 (20.3) | 52 (24.3) | 0.34 |
| CAD, n (%) | 43 (23.0) | 55 (25.7) | 0.53 |
| MI, n (%) | 17 (9.1) | 28 (13.1) | 0.21 |
| Prior Stroke, n (%) | 11 (5.9) | 23 (10.7) | 0.08 |
| Tobacco use, n (%) | 38 (20.3) | 38 (9.5) | 0.51 |
| Any alcohol use, n (%) | 66 (35.3) | 79 (36.9) | 0.74 |
| SBP, mm Hg (mean, SD) | |||
| Prehospital | 157 (26.1) | 156 (25.0) | 0.76 |
| ED Arrival | 157 (25.1) | 154 (25.9) | 0.49 |
| Early ED Course | 146 (22.8) | 144 (23.4) | 0.85 |
| DBP, mm Hg (mean, SD) | |||
| Prehospital | 87 (15.9) | 88 (18.6) | 0.13 |
| ED Arrival | 84 (18.5) | 82 (16.5) | 0.22 |
| Early ED Course | 76 (16.4) | 75 (17.2) | 0.61 |
| Prehospital GCS, median (IQR) | |||
| Median (IQR) | 15 (12-15) | 15 (12-15) | 0.76 |
| Mean (SD) | 13.7 (1.9) | 13.6 (2.5) | 0.71 |
| Prehospital LAMS | |||
| Median (IQR) | 4 (3-5) | 5 (3-5) | 0.95 |
| Mean (SD) | 4.1 (1.0) | 4.1 (1.1) | 0.50 |
| Blood Serum Mg Level at 72 h (mEq/L) Mean (SD) | 1.9 (0.37) | 3.6 (1.1) | <0.001 |
In the neuroprotectant Magnesium treatment group, the median time from last known well (LKW) to the start of Mg infusion was 46 (IQR 35-64) min. The median time from LKW to ED arrival was 56 (IQR 46-76) min and to TPA administration was 150 (IQR 124-171) min. The time from study drug administration to ED arrival was 10 (IQR 5-14) min. The time from ED arrival to the first scan was 25 (IQR 17-34) min and from ED arrival to TPA was 83 (IQR 62-106) min. The duration of neuroprotectant exposure was quantified as the median time from Mg administration to TPA, which was 93 (IQR 75-117) min. There were no significant differences between Magnesium and Placebo study groups in any of the time metrics (Table 2).
Table 2.
Time intervals TPA.
| Characteristics Median (IQR) | TPA + Pl (n = 187) |
TPA + Mg (n = 214) |
P- value |
|---|---|---|---|
| LKWT to Study Drug Administration | 45 (36-63) | 46 (35-64) | 0.89 |
| LKWT to ED Arrival | 56 (46-75) | 56 (46-76) | 0.87 |
| LKWT to TPA | 145 (126-168) | 150 (124-171) | 0.62 |
| Study Drug to ED Arrival | 10 (6-14) | 10 (5-14) | 0.95 |
| ED Arrival to First Scan | 25 (17-34) | 25 (17-34) | 0.79 |
| ED Arrival to TPA | 78 (62-102) | 83 (62-106) | 0.44 |
| Study Drug Administration to TPA | 90 (75-122) | 93 (75-117) | 0.46 |
Clinical outcome at Day 4 and Day 90 were analyzed by brackets of NIHSS at hospital arrival (≤8, 9–15, and >15). In a subgroup of patients with NIHSS ≤8, TPA+Mg group showed outcome scores that were significantly better compared to TPA+Pl group in Day 4 GCS (Mg 15 ±0.3 vs Pl 14.1 ± 2.4, p < 0.001) and Day 4 NIHSS (Mg 4.1 ± 4.7 vs Pl 5.7 ± 8.4, p = 0.04). In a subgroup of patients with NIHSS 9-15, TPA+Mg group showed outcome scores that were significantly better compared to TPA+Pl group in Day 4 GCS (Mg 14.4 ± 1.8 vs Pl 13.4 ± 3.5, p < 0.001). There was also a trend towards better outcome on Day 4 NIHSS in TPA+Mg group vs TPA+Pl (Mg 7.7 ± 7.4 vs Pl 10.5 ± 11.0, P = 0.09). In a subgroup of patients with NIHSS >15, TPA+Mg group showed significantly higher Day 4 Barthel index compared to TPA+Pl (Mg 24.6 ± 34.3 vs Pl 14.0 ± 23.7, p < 0.001). There was no statistically significant difference in hemorrhagic transformation between the two study groups in all NIHSS bracket.
At 90 days, there was no significant change in functional outcome between the Mg and placebo group at NIHSS ≤8, and 9–15. In a subgroup of patients with NIHSS >15, TPA+Mg group had significantly more patients with mRS 0-2 (Mg 21, 28% vs 10, 14%, p = 0.04) and lower median LAMS score (Mg 3 IQR 1-5 vs Pl 4 IQR 1-5, p = 0.04) compared to TPA+Pl group. The 90-day mortality rate and NIHSS was not significantly different between the two groups in all NIHSS brackets. Ordinal shift analysis of 90-day mRS using proportional odds regression demonstrated no significant treatment effect (common OR 0.25, 95% CI-0.24 –1.43, p = 0.59) (Fig. 1).
Fig. 1.
Bar chart of functional outcomes between TPA+Placebo and TPA+Magnesium – Day 90 mRS.
Discussion
The strategy of prehospital NP start was effective in enabling the study agent to have a long bridging period of potential effect. Prehospital magnesium therapy in combination with TPA was safe but did not demonstrate a significant benefit in primary clinical outcomes. Stratified by baseline National Institutes of Health Stroke Scale (NIHSS ≤8, 9–15, >15), magnesium plus TPA in subgroup of NIHSS >15 had higher proportion with mRS 0-2 at 90 days, and lower median LAMS scores compared with placebo; however, these findings should be considered exploratory. These findings were not supported by overall 90-day outcomes mRS analysis, which showed no significant treatment effect or mortality difference between groups.
While some statistically significant differences were observed, the magnitude was small and should be interpreted cautiously. These subgroup findings, including the NIHSS > 15 results, are exploratory and hypothesis-generating; they should not be interpreted as evidence of treatment efficacy in the absence of a prospectively powered confirmatory analysis. Regarding the observed LAMS difference in the NIHSS > 15 subgroup (median 3 vs. 4, p = 0.04), while statistically significant, the one-point difference on a 0-5 scale represents a small absolute magnitude, and its clinical relevance remains uncertain and warrants further investigation.
Compared with trials of in-hospital start of NP agents, the duration of brain-under-protection, between agent start and thrombolysis start, was substantially longer in FAST-MAG. For example, in the recent ESCAPE-NA1 trial, the study neuroprotective infusion was not started until after thrombolytic start in the patients receiving thrombolysis.17 When patients first arrive at hospital, the initial focus is on start of clinically proven agents such as thrombolytics. Patients are rushed to imaging and then the first consent conversation is started regarding clinical consent for thrombolysis. Often only after the lytic decision has been made and steps to start lytics are under way is there an opportunity to have a research consent conversation for a study drug. In contrast, the prehospital setting offers a window in which consent can be obtained or agent started under emergency exception from informed consent research regulations well ahead of these in-hospital events. Additionally, due to rural-urban disparities, transport times and time to TPA vary widely across the United States and the world and it is possible that scenarios allow for longer neuroprotective-to-thrombolysis bridge exposure.
Possible explanations for the full scope of the results of this study include that Mg is not an optimal neuroprotectant in humans,13 or that the duration of exposure of Mg prior to TPA was not long enough. Analysis of NP effects and duration with an agent such as Mg has a limitation in that Mg levels in the cerebrospinal fluid have been shown to peak around 4 h18 (within a similar dose range) whereas the median exposure time of Mg prior to TPA administration was 92 min. Due to this delayed trafficking of Mg across the blood-brain barrier, there may not have been enough drug present within the brain tissues to have a clinical impact. Due to the current indicated use of TPA within 4.5 h of stroke symptom onset, it is unlikely that a clinical trial would be able to coordinate administration of Mg quickly enough to allow for the exposure time to be closer to the optimal 4-hour period, while still within the window of TPA administration.
This study is a secondary analysis of the FAST-MAG Phase III randomized placebo-controlled clinical trial, which demonstrated the feasibility of prehospital neuroprotectant administration in the field but did not meet its primary endpoint. Accordingly, the findings of this analysis should be interpreted with caution and considered exploratory and hypothesis-generating, pending confirmation in prospectively designed studies. Additionally, though the FAST-MAG trial entry criteria were very broad in age, stroke severity, and co-morbidities13,14 the study did exclude patients with pre-stroke disability, systolic blood pressure higher than 220, and other uncommon features, constraining generalizability. Second, times from hospital arrival to thrombolytic start have improved somewhat since trial performance which would mildly reduce the bridging dwell time of a prehospital NP agent. Third, follow-up perfusion or angiographic imaging after thrombolysis was not routinely obtained, preventing separate analysis of reperfusers and non-reperfusers. An additional limitation relates to the evolving standard of care in thrombolysis. As this study utilized alteplase, and clinical practice has increasingly shifted toward tenecteplase,19 the extent to which these findings generalize to current treatment approaches remains uncertain.
An important consideration in systemic neuroprotective strategies for acute ischemic stroke is the extent to which therapeutic agents can reach hypoperfused tissue distal to an arterial occlusion. Although complete cessation of flow occurs in the infarct core, most patients retain some degree of collateral circulation that sustains perfusion to the ischemic penumbra.20 This residual blood flow, while reduced, can be to some extent sufficient to permit delivery of systemically administered agents to at-risk tissue.21 In addition, the ultra-early, prehospital administration paradigm employed in the FAST-MAG Phase III randomized controlled trial likely enables drug delivery at a time when tissue viability and perfusion are still partially preserved. Furthermore subsequent reperfusion—whether spontaneous or treatment-induced—may enhance drug penetration into previously ischemic regions, supporting a potential role for early ‘priming’ of vulnerable tissue.22 Together, these factors provide a physiological basis for the effectiveness of systemic neuroprotective strategies despite the presence of large vessel occlusion. However, the degree and consistency of drug delivery to severely hypoperfused regions remain variable and requires further understanding. Furthermore, given the number of subgroup analyses and secondary endpoints evaluated across NIHSS severity strata, the probability of type 1 error is elevated. Readers should interpret all secondary and subgroup findings with appropriate caution, recognizing that these analyses were not pre-specified with formal corrections for multiple comparisons.
Conclusion
Prehospital magnesium followed by alteplase was feasible and safe but did not demonstrate a significant overall clinical benefit. The main contribution of this analysis is to quantify the substantial prereperfusion exposure interval achievable with prehospital neuroprotective therapy, supporting this model for future agents requiring early biological exposure before reperfusion.
Supplementary Material
Supplementary material associated with this article can be found, in the online version, at doi:10.1016/j.jstrokecerebrovasdis.2026.108709.
Acknowledgement
The authors thank FAST-MAG Investigators and Coordinators. The authors also thank Sindhu Daggupati for her assistance with the final revisions of the manuscript.
Funding sources
This funding was supported by NIH—NINDS Award U01 NS 44364.
Footnotes
Statement of ethics
The study (ClinicalTrials.gov Identifier: NCT00059332) was approved by the Institutional Review Board (IRB) at the leading institution.
AI statement
During the preparation of this work the author(s) used ChatGPT 5.0 for manuscript review the text refinement. After using this tool/service, the authors reviewed and edited the content as needed and take full responsibility for the content of the publication.
CRediT authorship contribution statement
Kristina Shkirkova: Writing – original draft, Visualization, Validation, Formal analysis, Data curation. Sokena Zaidi: Writing – original draft, Validation. May A. Kim-Tenser: Writing – review & editing, Supervision, Resources, Methodology, Investigation, Conceptualization. Manuel Morales: Writing – review & editing, Validation. Kristina Van De Goor: Writing – original draft, Methodology, Formal analysis. David S. Liebeskind: Writing – review & editing, Validation, Supervision, Funding acquisition, Conceptualization. Scott Hamilton: Writing – review & editing, Supervision, Formal analysis, Data curation. Jeffrey L. Saver: Validation, Supervision, Resources, Project administration, Methodology, Investigation, Funding acquisition, Data curation. Nerses Sanossian: Writing – review & editing, Validation, Supervision, Resources, Project administration, Methodology, Investigation, Funding acquisition, Data curation, Conceptualization.
Declaration of competing interest
The authors report no conflicts of interest.
Data availability
The main FAST-MAG trial database and materials have been made publicly available at the NIH-NINDS Archived Clinical Research Datasets and can be accessed at https://www.ninds.nih.gov/Current-Research/Research-Funded-NINDS/Clinical-Research/Archived-Clinical-Research-Datasets.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Supplementary Materials
Data Availability Statement
The main FAST-MAG trial database and materials have been made publicly available at the NIH-NINDS Archived Clinical Research Datasets and can be accessed at https://www.ninds.nih.gov/Current-Research/Research-Funded-NINDS/Clinical-Research/Archived-Clinical-Research-Datasets.