High-definition transcranial direct current stimulation for upper extremity rehabilitation in moderate-to-severe ischemic stroke: a pilot study.

Introduction: Previous studies found that post-stroke motor impairments are associated with damage to the lesioned corticospinal tract (CST) and hyperexcitability of the contralesional cortico-reticulospinal tract (CRST). This proof-of-concept study aims to develop a non-invasive brain stimulation protocol that facilitates the lesioned CST and inhibits the contralesional CRST to improve upper extremity rehabilitation in individuals with moderate-to-severe motor impairments post-stroke. Methods: Fourteen individuals (minimum 3 months post ischemic stroke) consented. Physician decision of the participants baseline assessment qualified eight to continue in a randomized, double-blind cross-over pilot trial (ClinicalTrials.gov Identifier: NCT05174949) with: (1) anodal high-definition transcranial direct stimulation (HD-tDCS) over the ipsilesional primary motor cortex (M1), (2) cathodal HD-tDCS over contralesional dorsal premotor cortex (PMd), (3) sham stimulation, with a two-week washout period in-between. Subject-specific MR images and computer simulation were used to guide HD-tDCS and verified by Transcranial Magnetic Stimulation (TMS) induced Motor Evoked Potential (MEP). The motor behavior outcome was evaluated by an Fugl-Meyer Upper Extremity score (primary outcome measure) and the excitability of the ipslesoinal CST and contralesional CRST was determined by the change of MEP latencies and amplitude (secondary outcome measures). Results: The baseline ipsilesional M1 MEP latency and amplitude were correlated with FM-UE. FM-UE scores were improved post HD-tDCS, in comparison to sham stimulation. Both anodal and cathodal HD-tDCS reduced the latency of the ipsilesional M1 MEP. The contralesional PMd MEP disappeared/delayed after HD-tDCS. Discussion: These results suggest that HD-tDCS could improve the function of the lesioned corticospinal tract and reduce the excitability of the contralesional cortico-reticulospinal tract, thus, improving motor function of the upper extremity in more severely impaired individuals.

Discovery and validation of circulating stroke metabolites by NMR-based analyses using patients from the MISS and UK Biobank.

BACKGROUND: Stroke is a significant health issue in the United States, and identifying biomarkers for the prevention and functional recovery after an acute stroke remains the highest priority. This study aims to identify circulating metabolite signatures that may be associated with stroke pathophysiology by performing discovery and validation studies. METHODS: We performed targeted metabolomics profiling of 420 participants of the discovery dataset of Metabolome in an Ischemic Stroke Study (MISS) using high-throughput nuclear magnetic resonance (NMR) spectroscopy. A validation study of significantly altered metabolites was conducted using an independent cohort of 117,988 participants from the UK Biobank, whose metabolomics profiles were generated using the same NMR technology. RESULTS AND CONCLUSION: Our study identified 16 metabolites to be significantly perturbed during acute stroke. Amino acid phenylalanine was significantly increased, while glutamine and histidine were significantly lowered in stroke. Serum levels of apolipoprotein A-1, HDL particles, small HDL particles, essential fatty acids, and phosphatidylcholine were reduced, while ketone bodies like 3-hydroxybutyrate and acetoacetate were markedly increased in stroke. Based on the robust validation in a large independent UK Biobank dataset, some of these analytes may become clinically meaningful biomarkers to predict or prevent stroke in humans.

Difference in acute and chronic stage ischemic stroke metabolic markers with controls.

BACKGROUND: Acute Ischemic Stroke (AIS), a major cause of disability, was previously associated with multiple metabolomic changes, but many findings were contradictory. Case-control and longitudinal study designs could have played a role in that. To clarify metabolomic changes, we performed a simultaneous comparison of ischemic stroke metabolome in acute, chronic stages of stroke and controls. METHODS: Through the nuclear magnetic resonance (NMR) platform, we evaluated 271 serum metabolites from a cohort of 297 AIS patients in acute and chronic stages and 159 controls. We used Sparse Partial Least Squares-Discriminant analysis (sPLS-DA) to evaluate group disparity; multivariate regression to compare metabolome in acute, chronic stages of stroke and controls; and mixed regression to compare metabolome acute and chronic stages of stroke. We applied false discovery rate (FDR) to our calculations. RESULTS: The sPLS-DA revealed separation of the metabolome in acute, chronic stages of stroke and controls. Regression analysis identified 38 altered metabolites. Ketones, branched-chain amino acids (BCAAs), energy, and inflammatory compounds were mostly elevated, while alanine and glutamine were decreased in the acute stage. These metabolites declined/increased in the chronic stage, often to the same levels as in controls. Levels of fatty acids, phosphatidylcholines, phosphoglycerides, and sphingomyelins did not change between acute and chronic stages, but were different comparing to controls. CONCLUSION: Our pilot study identified metabolites associated with acute stage of ischemic stroke and those that are altered in stroke patients comparing to controls regardless of stroke acuity. Future investigation in a larger independent cohort is needed to validate these findings.

Comparison of Acute and Chronic Stage Ischemic Stroke Metabolome with Controls.

Background: Acute Ischemic Stroke (AIS), a major cause of disability, was previously associated with multiple metabolomic changes, but many findings were contradictory. Case-control and longitudinal study designs could have played a role in that. To clarify metabolomic changes, we performed a simultaneous comparison of ischemic stroke metabolome in acute, chronic stages of stroke and controls. Methods: Through the nuclear magnetic resonance (NMR) platform, we evaluated 271 serum metabolites from a cohort of 297 AIS patients in acute and chronic stages and 159 controls. We used Sparse Partial Least Squares-Discriminant analysis (sPLS-DA) to evaluate group disparity; multivariate regression to compare metabolome in acute, chronic stages of stroke and controls; and mixed regression to compare metabolome acute and chronic stages of stroke. We applied false discovery rate (FDR) to our calculations. Results: The sPLS-DA revealed separation of the metabolome in acute, chronic stages of stroke and controls. Regression analysis identified 38 altered metabolites. Ketone bodies, branched-chain amino acids (BCAAs), energy, and inflammatory compounds were elevated in the acute stage, but declined in the chronic stage, often to the same levels as in controls. Levels of other amino acids, phosphatidylcholines, phosphoglycerides, and sphingomyelins mainly did not change between acute and chronic stages, but was different comparing to controls. Conclusion: Our pilot study identified metabolites associated with acute stage of ischemic stroke and those that are altered in stroke patients comparing to controls regardless of stroke acuity. Future investigation in a larger independent cohort is needed to validate these findings.

Predictors of Atrial Fibrillation in Patients With Stroke Attributed to Large- or Small-Vessel Disease: A Prespecified Secondary Analysis of the STROKE AF Randomized Clinical Trial.

Importance: The Stroke of Known Cause and Underlying Atrial Fibrillation (STROKE AF) trial found that approximately 1 in 8 patients with recent ischemic stroke attributed to large- or small-vessel disease had poststroke atrial fibrillation (AF) detected by an insertable cardiac monitor (ICM) at 12 months. Identifying predictors of AF could be useful when considering an ICM in routine poststroke clinical care. Objective: To determine the association between commonly assessed risk factors and poststroke detection of new AF in the STROKE AF cohort monitored by ICM. Design, Setting, and Participants: This was a prespecified analysis of a randomized (1:1) clinical trial that enrolled patients between April 1, 2016, and July 12, 2019, with primary follow-up through 2020 and mean (SD) duration of 11.0 (3.0) months. Eligible patients were selected from 33 clinical research sites in the US. Patients had an index stroke attributed to large- or small-vessel disease and were 60 years or older or aged 50 to 59 years with at least 1 additional stroke risk factor. A total of 496 patients were enrolled, and 492 were randomly assigned to study groups (3 did not meet inclusion criteria, and 1 withdrew consent). Patients in the ICM group had the index stroke within 10 days before insertion. Data were analyzed from October 8, 2021, to January 28, 2022. Interventions: ICM monitoring vs site-specific usual care (short-duration external cardiac monitoring). Main Outcomes and Measures: The ICM device automatically detects AF episodes 2 or more minutes in length; episodes were adjudicated by an expert committee. Cox regression multivariable modeling included all parameters identified in the univariate analysis having P values <.10. AF detection rates were calculated using Kaplan-Meier survival estimates. Results: The analysis included the 242 participants randomly assigned to the ICM group in the STROKE AF study. Among 242 patients monitored with ICM, 27 developed AF (mean [SD] age, 66.6 [9.3] years; 144 men [60.0%]; 96 [40.0%] women). Two patients had missing baseline data and exited the study early. Univariate predictors of AF detection included age (per 1-year increments: hazard ratio [HR], 1.05; 95% CI, 1.01-1.09; P = .02), CHA2DS2-VASc score (per point: HR, 1.54; 95% CI, 1.15-2.06; P = .004), chronic obstructive pulmonary disease (HR, 2.49; 95% CI, 0.86-7.20; P = .09), congestive heart failure (CHF; with preserved or reduced ejection fraction: HR, 6.64; 95% CI, 2.29-19.24; P < .001), left atrial enlargement (LAE; HR, 3.63; 95% CI, 1.55-8.47; P = .003), QRS duration (HR, 1.02; 95% CI, 1.00-1.04; P = .04), and kidney dysfunction (HR, 3.58; 95% CI, 1.35-9.46; P = .01). In multivariable modeling (n = 197), only CHF (HR, 5.06; 95% CI, 1.45-17.64; P = .05) and LAE (HR, 3.32; 1.34-8.19; P = .009) remained significant predictors of AF. At 12 months, patients with CHF and/or LAE (40 of 142 patients) had an AF detection rate of 23.4% vs 5.0% for patients with neither (HR, 5.1; 95% CI, 2.0-12.8; P < .001). Conclusions and Relevance: Among patients with ischemic stroke attributed to large- or small-vessel disease, CHF and LAE were associated with a significantly increased risk of poststroke AF detection. These patients may benefit most from the use of ICMs as part of a secondary stroke prevention strategy. However, the study was not powered for clinical predictors of AF, and therefore, other clinical characteristics may not have reached statistical significance. Trial Registration: ClinicalTrials.gov Identifier: NCT02700945.

Cortical Reorganization of Early Somatosensory Processing in Hemiparetic Stroke.

The cortical motor system can be reorganized following a stroke, with increased recruitment of the contralesional hemisphere. However, it is unknown whether a similar hemispheric shift occurs in the somatosensory system to adapt to this motor change, and whether this is related to movement impairments. This proof-of-concept study assessed somatosensory evoked potentials (SEPs), P50 and N100, in hemiparetic stroke participants and age-matched controls using high-density electroencephalograph (EEG) recordings during tactile finger stimulation. The laterality index was calculated to determine the hemispheric dominance of the SEP and re-confirmed with source localization. The study found that latencies of P50 and N100 were significantly delayed in stroke brains when stimulating the paretic hand. The amplitude of P50 in the contralateral (to stimulated hand) hemisphere was negatively correlated with the Fügl-Meyer upper extremity motor score in stroke. Bilateral cortical responses were detected in stroke, while only contralateral cortical responses were shown in controls, resulting in a significant difference in the laterality index. These results suggested that somatosensory reorganization after stroke involves increased recruitment of ipsilateral cortical regions, especially for the N100 SEP component. This reorganization delays the latency of somatosensory processing after a stroke. This research provided new insights related to the somatosensory reorganization after stroke, which could enrich future hypothesis-driven therapeutic rehabilitation strategies from a sensory or sensory-motor perspective.

Global Metabolomic Profiling Reveals Disrupted Lipid and Amino Acid Metabolism Between the Acute and Chronic Stages of Ischemic Stroke.

BACKGROUND: Stroke is a major cause of serious disability in the United States. Previous studies found multiple associations of serum metabolites with acute ischemic stroke (AIS) compared to controls, but few of them evaluated metabolome in a longitudinal fashion. Therefore, we compared the metabolome of the acute and chronic stages of ischemic stroke. METHODS: We evaluated 1295 serum metabolites from the cohort of 60 stroke patients at acute and chronic stages by performing global metabolomics using ultra-high-performance liquid chromatography/mass spectrometry (LC-MS) and gas chromatography/mass spectrometry (GC-MS). We used Orthogonal Partial Least Square-Discrimination Analysis (OPLS-DA) to inspect group disparity and a mixed regression model to compare metabolites in the acute and chronic stages with Two-Stage Benjamini & Hochberg (TSBH) and Bonferroni correction for multiple testing. RESULTS: The OPLS-DA revealed significant separation of acute and chronic stage metabolites. Mixed regression identified 228 metabolites with TSBH, and 29 metabolites with Bonferroni correction different in acute and chronic stages. At the acute stage, there was a consistent increase of the metabolites of mono/diacylglycerols, sphingolipids, medium/long-chain fatty acids, and amino acids glycine, valine, and tyrosine. At the same time, there was a consistent decrease of the metabolites of acyl-choline related fatty acids, phospholipids, and amino acids alanine, aspartate, and tyramine. Additionally, we identified eight novel metabolites significantly altered at the acute stage of stroke. CONCLUSION: Our pilot study demonstrated significant alterations in metabolomic patterns between the acute and chronic stages of stroke, validating some case-control findings. Future investigation in a larger independent cohort is warranted to identify early biomarkers of acute ischemic stroke.

Quantitative Analysis of Stress-Induced Hyperglycemia and Intracranial Blood Volumes for Predicting Mortality After Intracerebral Hemorrhage.

Stress-induced hyperglycemia (SIH) is a neuroendocrine response to acute illness. Although SIH has an adverse association with intracerebral hemorrhage (ICH), quantitative measures and determinants of SIH are not well delineated. In the present study, we objectively evaluated SIH using glycemic gap (GG) and identified its radiological and clinical determinants, with a 5-year retrospective review of charts of ICH patients. We calculated GG using the regression equation (GG = AG -28.7 × HbA1c + 46.7) and evaluated whether GG is an independent predictor of mortality using a multivariate regression model. Radiological volumes of different intracranial compartments were determined using image segmentation software. We correlated GG with different clinical and radiological parameters using Pearson correlation coefficient (PCC), Spearman's rank correlation (SRC), and Wilcoxon rank sum test. Then, we calculated the value of GG associated with mortality. Out of 328 patients, 238 (73%) survived hospitalization and 90 (27%) expired. GG was found to be an independent predictor of mortality (r=0.008, p=0.04). Additionally, GG was positively correlated with intraparenchymal hemorrhage (IPH) volume (PCC=0.185, p<0.01) and intraventricular hemorrhage (IVH) volume (PCC=0.233, p<0.01) and negatively correlated with cerebrospinal fluid (CSF) volume (PCC=-0.151, p<0.01) and brain tissue volume (PCC=-0.099, p=0.08). GG was positively correlated with patients' ICH score (SRC=0.377, p<0.01), Glasgow Coma Scale (GCS) (PCC=-0.356, p<0.01), hydrocephalus (p<0.01), and IVH in the third ventricle (p<0.01). The univariate logistic regression model identified 30.0 mg/dl as the value of GG (AUC=0.655, p<0.01) that predicted mortality with 52.2% sensitivity and 75.2% specificity and defined SIH. In conclusion, GG independently predicts mortality in ICH patients and positively correlates with IPH and IVH volumes. However, causality between the two is not established and would require specifically designed studies.

Novel Metabolites as Potential Indicators of Ischemic Infarction Volume: a Pilot Study.

Metabolomics may identify biomarkers for acute ischemic stroke (AIS). Previously, circulating metabolites were compared in AIS and healthy controls without accounting for stroke size. The goal of this study was to identify metabolites that associate with the volume of AIS. We prospectively analyzed 1554 serum metabolites in the acute (72 h) and chronic (3-6 months) stages of 60 ischemic stroke patients. We calculated infarct volume using diffusion-weighted images with MR segmentation software and associated the volume with stage-specific metabolites, acute-to-chronic stage changes, and multiple mixed regression in metabolite concentrations using multivariate regression analysis. We used the two-stage Benjamini and Hochberg (TSBH) procedure for multiple testing. Four unknown metabolites at the acute stage significantly associated with infarct volume: X24541, X24577, X24581, and X2482 (all p < 0.01). Nine metabolites at the chronic stage are significantly associated with infarct volume: indolpropinate, alpha ketoglutaramate, picolinate, X16087, X24637, X24576, X24577, X24582, X24581 (all p < 0.048). Infarct volume is also associated with significant changes in serum concentrations of twenty-seven metabolites, with p values from 0.01 to 1.48 × 10-7, and on five metabolites using mixed regression model. This prospective pilot study identified several metabolites associated with the volume of ischemic infarction. Confirmation of these findings on a larger dataset would help characterize putative pathways underlying the size of ischemic infarction and facilitate the identification of biomarkers or therapeutic targets.

Predicting Clinical Outcome After Mechanical Thrombectomy: The GADIS (Gender, Age, Diabetes Mellitus History, Infarct Volume, and Current Smoker [corrected]) Score.

OBJECTIVE: To investigate predictive factors and develop an outcome assessment tool to determine clinical outcome after endovascular mechanical thrombectomy (EMT) in patients presenting with large vessel occlusion (LVO). METHODS: A retrospective analysis was carried out of a prospective cohort of patients presenting with LVO who underwent EMT after adoption of an expanded time window of ≤24 hours. Final cerebral infarction volume (CIV) after EMT was estimated using magnetic resonance imaging segmentation software. Stepwise linear regression models were used to identify factors that determined clinical outcome and to develop a predictive scale. RESULTS: Ninety patients underwent EMT over 19 months (68 within 6 hours and 22 between 6 and 24 hours). Clinical outcome determined using modified Rankin Scale (mRS) score at discharge and 3 months was no different among these subcohorts. A threshold of 16.99 mL of CIV, using the Youden index, resulted in a sensitivity of 90.5% and specificity of 58.1% for predicting mRS score of 0-2. A regression model identified gender, age, diabetes mellitus status, CIV, and smoking status as outcome determinants, which were used to develop the GADIS (Gender, Age, Diabetes Mellitus History, Infarct Volume, and Sex) scoring system to predict good clinical outcome. Using the GADIS score, <6 predicted mRS score 0-2 at discharge with a sensitivity of 83.3% and specificity of 80.6%. CONCLUSIONS: The GADIS score for patients with LVO-related acute ischemic stroke includes CIV after EMT and helps in early short-term prognostication. It is not intended to predict preintervention patient selection or outcome prediction.

Trends of Platelet Volume Index Predicts Delayed Cerebral Ischemia After Subarachnoid Hemorrhage.

BACKGROUND: Delayed cerebral ischemia (DCI) is a major cause of disability after aneurysmal subarachnoid hemorrhage (aSAH). Activated platelets are surrogate markers for DCI occurrence and are reliably represented by mean platelet volume (MPV) to platelet count (PLT) ratio. If validated as a predictor of DCI, the ratio will allow clinicians to use it as a readily available tool in patient management. METHODS: Retrospective analysis of aSAH patient database at a tertiary care hospital. MPV:PLT ratio was defined as (MPV value(fL)PLT per 1000∗100). Nonlinear regression estimated differences in the ratio's pattern of change over time between those with or without DCI. Receiver operating characteristic curve determined optimal threshold of rise in MPV:PLT ratio to predict DCI. RESULTS: Average age of the cohort (n = 169) was 53.0 ± 13.0 years, and 38 patients (22.5%) developed DCI. Nonlinear regression analysis detected a transition of rising and declining MPV:PLT ratio at 3 days after aSAH. Rate of rise in MPV:PLT ratio was 0.5 units/day (95% confidence interval 0.3-0.7) in patients developing DCI as compared with 0.2 units/day (95% confidence interval 0.1-0.3) in those without DCI (P = 0.0004). Receiver operating characteristic analysis determined a threshold of 0.33 units/day rise in MPV:PLT predicted DCI with 89.5% sensitivity and 90.8% specificity. Patients who died demonstrated a steeper rise during the first 3 days (0.29 units/day) than those who were discharged home (0.21 units/day) (P = 0.004). CONCLUSIONS: Trend of MPV:PLT ratio after aSAH predicts DCI. This association alludes to significant early rise in reactive platelet population after aSAH in patients developing DCI.

Cost-Minimization Analysis of Computed Tomography versus Magnetic Resonance Imaging in the Evaluation of Patients with Transient Ischemic Attacks at a Large Academic Center.

BACKGROUND: The type of neuroimaging for the evaluation of transient ischemic attack (TIA) is debatable. Many patients undergo head computed tomography (CT) with or without CT angiogram (CTA) while being at the emergency department (ED) and later magnetic resonance imaging (MRI) with MR angiogram (MRA) during admission. We hypothesized that evaluation with only one imaging modality (CT/CTA or MRI/MRA) is sufficient to formulate a treatment plan. We looked for the most cost-effective way to evaluate TIA patients. METHODS: We performed a retrospective chart review of 82 patients with TIA. All patients had completely resolved neurological deficit at the time of their evaluation in the ED. We divided the patients into two groups. In group 1, the evaluation included CT with CTA of the head and neck. In group 2, the evaluation included brain MRI with MRA or CTA of the head and neck. We compared these two groups for clinical characteristics and etiological evaluations of stroke/TIA. The outcomes were measured by the number of therapeutic adjustments for the prevention of another ischemic stroke/TIA at the time of discharge from the hospital and revascularization procedures. We counted the following as therapeutic adjustment: (1) antiplatelet therapy was started de novo; (2) anticoagulation was started; (3) arterial revascularization procedure was performed, and (4) one antiplatelet agent was substituted for another. We performed a cost-effectiveness analysis if the outcomes of the two groups were different and a cost-minimization analysis if there was no difference in the outcomes. All cost calculations were made based on Medicare CPT codes. RESULTS: Group 1 included 23 patients and group 2 59 patients. The patients in both groups had similar demographic and clinical characteristics. There was no difference in other etiological evaluations in groups 1 and 2. All patients underwent head CT as the first tool of evaluation whether MRI was done later or not. Therapeutic adjustments and revascularization procedures did not differ between the two groups. All head CTs showed no acute changes. MRI showed small ischemic infarcts in 44% of the patients in group 2. The average per-patient cost of neuroimaging with CT/CTA was USD 1,460.00, with CT and MRI/MRA USD 1,569 and with CT/CTA and brain MRI USD 2,090.00 (p < 0.01). CONCLUSION: Either MRI/MRA or CT/CTA might be sufficient for the evaluation of patients with TIA or small asymptomatic strokes. If head CT at the ED is bypassed, a brain MRI with MRA of the head and neck would be the most informative tool at the lowest cost. Prospective studies with larger numbers of patients are needed for a better understanding of the safety and cost of imaging tools used for patients with TIA.

Hyperglycemia and outcome in intracerebral hemorrhage: from bedside to bench-more study is needed.

Hyperglycemia on admission has been associated with poor outcome after intracerebral hemorrhage (ICH). However, the mechanistic links between hyperglycemia and poor outcome are not fully elucidated. We sought to determine the relationship between the serum glucose levels during the first 72 h after ICH, and evolution of hematoma and perihematomal edema (PHE), and functional outcome at 3 months and performed a retrospective review of prospectively collected data from 135 consecutive ICH patients. Patients were divided into two groups based on their mean glucose level-high (≥150 mg/dl) vs. controlled (<150 mg/dl). We used Chi-square test and multiple logistic regressions to assess the relationship between glucose level and outcome variables, including hematoma expansion (HE), PHE growth, and modified Rankin Scale (mRS) score at 3 months. The mean 72-h glucose level was 123 ± 16 for the controlled group and 190 ± 48 mg/dl for the high-glucose group. The corresponding rates of HE were 23.4 vs. 25.9 % (unadjusted p = 0.80; adjusted p = 0.08); PHE growth, 31.3 vs. 29.6 % (unadjusted p = 0.88; adjusted p = 0.39); and poor outcome at 3 months, defined as mRS score of ≥3, was 54 vs. 71 % (unadjusted p = 0.06; adjusted p = 0.89). On multivariate analyses, the ICH score emerged as the major predictor for poor outcome, but not glucose. In conclusion, we found a trend for an association between mean 72 h glucose levels and poor outcome at 3 months, but this effect attenuated after adjusting for the ICH score. High glucose was not associated with HE or PHE growth. More preclinical and clinical studies are needed to elucidate the role of hyperglycemia in ICH before embarking on large and costly clinical trials of tight glucose control in ICH patients.

Stroke in pregnant and postpartum women.

Ischemic infarcts and hemorrhages are uncommon but dangerous complications of pregnancy. Their etiology is related to physiological changes during pregnancy. The majority of strokes are seen in the third trimester and postpartum and are etiologically related to three conditions: reversible cerebral vasoconstriction syndrome, preeclampsia/eclampsia and cerebral venous thrombosis. The first two conditions are etiologically connected and can lead to ischemic and hemorrhagic events, whereas cerebral sinus thrombosis is mainly related to hypercoagulation and causes venous infarcts and brain hemorrhages. MRI and CT scans are safe to use for diagnosis of stroke in pregnancy, although use of iodine-based contrast may affect thyroid function of the neonate. Management of stroke in pregnancy is specific to cause and depends on management of blood pressure and delivery in preeclampsia/eclampsia, expected management or calcium channel blockers in reversible cerebral vasoconstriction syndrome, and anticoagulation for cerebral sinus thrombosis.