Abstract

Background: Methamphetamine (MA) abuse is an increasing worldwide epidemic with associations to acute ischemic strokes (AIS); however, exact effects have been underreported. In this single center study, we characterize effects of MA on AIS in terms of demographics, presentation, and clinical significance. Methods: We performed a retrospective analysis of 654 patients admitted to UC Davis Medical Center from 2016-2017 with primary diagnosis of AIS. Patients’ presenting characteristics, suspected stroke etiologies based on TOAST criteria, and clinical outcomes were compared between AIS with and without positive urine drug screen for MA. Results: Fifty patients with methamphetamine positive (MA+) AIS and 252 patients with methamphetamine negative (MA-) AIS were identified. MA+ AIS were predominantly male (0.78 vs 0.50, p=0.005) and significantly younger (56.2 vs 69.7, p<0.001) compared to MA-AIS. In general, patients with MA+ had a more severe presentation with higher systolic pressures (175.1 vs 157.6, p<0.001) and diastolic pressures (105 vs 86.23, p<0.001). Overall, the two groups did not differ in terms of presenting NIHSS, rates of TPA administration, length of stay, or ICU length of stay. In terms of etiologies, MA+AIS had significantly higher incidence of small vessel strokes (0.41 vs 0.20, p= 0.0017) whereas large vessel occlusions were significantly more predominant in MA-AIS (0.22 vs 0.10, p=0.04). Analysis of MRI burden of deep white matter (DWM) lesions based on Fazekas scale demonstrated significantly lower proportion of moderate to severe disease burn in MA +AIS (0.17 vs 0.49, p=0.0001). Overall, MA+AIS trended to an improved modified rankin scale at discharge, however this was not statistically significant. Conclusion: There is an earlier age of onset with significantly higher presenting blood pressures in MA+AIS and interestingly similar initial NIHSS, length of ICU stay, and hospital stay compared to MA-AIS. The majority of MA+AIS presented with small vessel strokes and significantly lower burden of deep white matter disease. This suggests that the cerebral small vessels may be more sensitive to the sympathomimetic nature of MA that may be driving transient hypertension and cerebral vasoconstriction as the potential pathogenesis.

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