Decrease of thyroid function after ischemic stroke is related to stroke severity.

BACKGROUND: Thyroid hormones are of fundamental importance for brain function. While low triiodothyronine levels during acute ischemic stroke (AIS) are associated with worse clinical outcomes, dynamics of thyroid function after AIS remains unknown. Thus, we longitudinally evaluated thyroid hormones after stroke and related them to stroke severity. METHODS: We prospectively traced thyroid stimulating hormone (TSH), free triiodothyronine (fT3), and free thyroxin (fT4) levels from the hyper-acute (within 24 h) to acute (3-5 days) and chronic (3-6 months) stages of ischemic stroke using a mixed regression model. Then, we analyzed whether stroke severity at presentation, expressed by National Institute of Health Stroke Scale (NIHSS), is associated with change in thyroid function. RESULTS: Forty-five patients were evaluated in hyper-acute and acute stages, while 29 were followed through chronic stage. TSH levels decreased from hyper-acute (2.91 ± 0.65 µIU/mL) to acute (2.86 ± 0.46 µIU/mL) and chronic stages of stroke (1.93 ± 0.35 µIU/m, p = 0.95). fT3 levels decreased from hyper-acute (2.79 ± 0.09 pg/ml) to acute (2.37 ± 0.07 pg/ml) stages, but recovered in chronic stage (2.78 ± 0.10 pg/ml, p < 0.01). fT4 levels decreased from hyper-acute (1.64 ± 0.14 ng/dl) to acute (1.13 ± 0.03 ng/dl) stages, and increased in the chronic stage (1.16 ± 0.08 ng/dl, p = 0.02). One-unit increase in presenting NIHSS was associated with 0.04-unit decrease of fT3 from hyper-acute to the acute stage (p < 0.01). CONCLUSION: There is a transient decrease of thyroid hormones after ischemic stroke, possibly driven by stroke severity. Larger studies are needed to validate these findings. Correction of thyroid function in acute stroke may be investigated to improve stroke outcomes.

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.

Diagnostic Yield of 8-Hour Video-EEG in Detecting Psychogenic Non-Epileptic Seizures (PNES).

To evaluate the diagnostic yield of the first 8 hours of video-EEG (vEEG) monitoring in detecting Psychogenic Non-Epileptic Seizures (PNES) during the Epilepsy Monitoring Unit (EMU) admission. We performed a retrospective chart review of patients ages ≥4 years who were admitted to the EMU between 2011 and 2018 (n = 616). We calculated the proportion of patients diagnosed with PNES within the first 8 hours of EEG recording and studied the associated risk factors for patients diagnosed with PNES and patients with epileptic seizures (ES). Out of the total 616 patients, 24% (149) patients had an EMU diagnosis of PNES. Of these, 44.3% had at least one typical event within the first 8 hours of vEEG monitoring. A higher incidence was seen within the pediatric subgroup (54.8% had an event within 8 hours). A diagnosis of chronic pain disorder was more common with PNES compared to ES (48.3% versus 16.5%, p < 0.001). A suspicion for PNES documented during an office visit was noted in a high proportion of patients (68.5%) who eventually had a PNES event during EMU. Our study suggests that in a well-selected group of patients (such as a high suspicion of PNES during a physician/neurology office visit), an outpatient 8-hour vEEG could open new avenues for a prompt diagnosis. This could especially be beneficial in hospital settings where there is either a lack of an EMU or a delay in admission to the EMU.

Systemic response of coated-platelet and peripheral blood inflammatory cell indices after aneurysmal subarachnoid hemorrhage and long-term clinical outcome.

PURPOSE: Post-hemorrhage period after aneurysmal subarachnoid hemorrhage (aSAH) has several systemic manifestations including prothrombotic and pro-inflammatory states. Inter-relationship between these states using established/routine laboratory biomarkers and its long-term effect on clinical outcome is not well-defined. MATERIALS AND METHODS: Retrospective analysis of prospective cohort of 44 aSAH patients. Trend of procoagulant biomarkers [coated-platelets, mean platelet volume to platelet count (MPV:PLT)] and peripheral inflammatory biomarkers [platelet-lymphocyte ratio (PLR), neutrophil-platelet ratio (NLR)] were analyzed using regression analysis. Occurrence of delayed cerebral ischemia (DCI), modified Rankin score (mRS) of 3-6 and Montreal cognitive assessment (MoCA) of <26 at 1-year defined adverse clinical outcome. RESULTS: Patients with worse mRS and MoCA score had higher rise in coated-platelet compared to those with better scores [20.4 (IQR: 15.6, 32.9) vs. 10.95 (IQR: 6.1, 18.9), p = 0.003] and [16.9 (IQR: 13.4, 28.1) vs. 10.95 (IQR: 6.35, 18.65), p = 0.02] respectively. NLR and PLR trends showed significant initial decline followed by a gradual rise in NLR among those without DCI as compared to persistent low levels in those developing DCI (0.13 units/day vs. -0.07 units/day, p = 0.06). CONCLUSIONS: Coated-platelet rise after aSAH is associated with adverse long-term clinical outcome. NLR and PLR trends show an early immune-depressed state after aSAH.