Hours Of Ischemic Stroke Research Articles

Longitudinal Evaluation of Resting-State fMRI After Acute Stroke With Hemiparesis

Background. Functional magnetic resonance imaging (fMRI) of motor impairment after stroke strongly depends on patient effort and capacity to make a movement. Hence fMRI has had limited use in clinical management. Alternatively, resting-state fMRI (ie, with no task) can elucidate the brain’s functional connections by determining temporal synchrony between brain regions. Objective. The authors examined whether resting-state fMRI can elucidate the disruption of functional connections within hours of ischemic stroke as well as during recovery. Methods. A total of 51 ischemic stroke patients—31 with mild-to-moderate hand deficits (National Institutes of Health Stroke Scale [NIHSS] motor score ≥1) and 20 with NIHSS score of 0—underwent resting-state fMRI at <24 hours, 7 days, and 90 days poststroke; 15 age-matched healthy individuals participated in 1 session. Using the resting-state fMRI signal from the ipsilesional motor cortex, the strength of functional connections with the contralesional motor cortex was computed. Whole-brain maps of the resting-state motor network were also generated and compared between groups and sessions. Results. Within hours poststroke, patients with motor deficits exhibited significantly lower connectivity than controls (P = .02) and patients with no motor impairment (P = .03). Connectivity was reestablished after 7 days in recovered (ie, NIHSS score = 0) participants. After 90 days, recovered patients exhibited normal motor connectivity; however, reduced connectivity with subcortical regions associated with effort and cognitive processing remained. Conclusion. Resting-state fMRI within hours of ischemic stroke can demonstrate the impact of stroke on functional connections throughout the brain. This tool has the potential to help select appropriate stroke therapies in an acute imaging setting and to monitor the efficacy of rehabilitation.

The Extent of Perfusion Deficit Does Not Relate to the Visibility of Acute Ischemic Lesions on Fluid‐Attenuated Inversion Recovery Imaging

Fluid-attenuated inversion recovery imaging (FLAIR) has been suggested as a surrogate marker of lesion age in acute ischemic stroke. In a subgroup analysis, we evaluated whether the extent of perfusion deficit influences FLAIR lesion visibility and thus plays a role as a confounding variable in the interpretation of FLAIR images. A subgroup of patients from a previous study evaluating the use of FLAIR imaging as a surrogate marker of lesion age within the first 6 hours of ischemic stroke were examined to determine the influence of the amount of perfusion deficit on FLAIR lesion visibility. N = 48 patients were included into the analysis. In positive and negative FLAIR lesion cases the extent of perfusion deficits did not differ significantly (150 mL vs. 197 mL, P = .730) nor influenced FLAIR visibility independently. In contrast, diffusion weighted imaging (DWI) lesion volumes were larger (34 mL vs. 14 mL, P = .008) and time from symptom onset longer (180 vs. 120 minute, P = .071) in FLAIR-positive cases. Visibility of FLAIR lesions in acute stroke imaging is influenced by lesion size and time from symptom onset to MRI, but not by the amount of perfusion deficit calculated by time-to-peak (TTP) measurements.

Blood‐Brain Barrier Na/HCO3 Cotransporters: Evidence for a Role in Ischemia‐induced Brain Na Uptake

Increased Na transport across the blood‐brain barrier (BBB) contributes to brain edema during the early hours of ischemic stroke. Our previous studies show that BBB Na‐K‐Cl cotransporter and Na/H exchange are stimulated by ischemic factors and inhibition of these Na transporters by bumetanide and HOE642, respectively, greatly attenuates Na uptake and edema in the rat middle cerebral artery occlusion (MCAO) model of stroke. In the present study, we examined the possibility that one or more Na/HCO3 cotransporters (NBCs) are present at the BBB and contribute to ischemia‐induced brain edema. NBC protein expression and activity were evaluated using Western blot and microspectroflurometric assays, respectively. We found the expression of NBCe1C and NBCn1 in bovine cerebral microvascular endothelial cells (CMEC) and freshly isolated rat brain microvessels. We also observed a Na‐ and HCO3‐dependent, HOE642‐insensitive H+ flux in CMEC that is comprised of both DIDS‐sensitive and DIDS‐insensitive components, indicating the presence of both NBCe1 and NBCn1 activity in the cells. Finally, localized 23Na MR spectroscopy was used to assess brain Na uptake in rats subjected to MCAO. We found that MCAO‐induced Na uptake was significantly reduced by DIDS (40 mg/kg, iv). These findings support the hypothesis that BBB NBCe1C and/or NBCn1 participate in ischemia‐induced brain Na uptake and edema formation.Supported by NINDS

Ischemia-induced stimulation of cerebral microvascular endothelial cell Na-K-Cl cotransport involves p38 and JNK MAP kinases.

Previous studies have provided evidence that, in the early hours of ischemic stroke, a luminal membrane blood-brain barrier (BBB) Na-K-Cl cotransporter (NKCC) participates in ischemia-induced cerebral edema formation. Inhibition of BBB NKCC activity by intravenous bumetanide significantly reduces edema and infarct in the rat permanent middle cerebral artery occlusion model of ischemic stroke. We demonstrated previously that the BBB cotransporter is stimulated by hypoxia, aglycemia, and AVP, factors present during cerebral ischemia. However, the underlying mechanisms have not been known. Ischemic conditions have been shown to activate p38 and JNK MAP kinases (MAPKs) in brain, and the p38 and JNK inhibitors SB-239063 and SP-600125, respectively, have been found to reduce brain damage following middle cerebral artery occlusion and subarachnoid hemorrhage, respectively. The present study was conducted to determine whether one or both of these MAPKs participates in ischemic factor stimulation of BBB NKCC activity. Cultured cerebral microvascular endothelial cell NKCC activity was evaluated as bumetanide-sensitive (86)Rb influx. Activities of p38 and JNK were assessed by Western blot and immunofluorescence methods using antibodies that detect total vs. phosphorylated (activated) p38 or JNK. We report that p38 and JNK are present in cultured cerebral microvascular endothelial cells and in BBB endothelial cells in situ and that hypoxia (7% O(2) and 2% O(2)), aglycemia, AVP, and O(2)-glucose deprivation (5- to 120-min exposures) all rapidly activate p38 and JNK in the cells. We also provide evidence that SB-239063 and SP-600125 reduce or abolish ischemic factor stimulation of BBB NKCC activity. These findings support the hypothesis that ischemic factor stimulation of the BBB NKCC involves activation of p38 and JNK MAPKs.

Autoimmune Responses to the Brain After Stroke Are Associated With Worse Outcome

Immune responses to brain antigens occur after stroke, and experimental studies show that the likelihood of developing a detrimental autoimmune response to these antigens is increased by systemic inflammation at the time of stroke. The aim of this study was to determine if patients who developed infection in the poststroke period would be similarly predisposed to develop autoimmune responses to central nervous system antigens. We enrolled 114 patients within 72 hours of ischemic stroke. Clinical and demographic data were obtained, and cellular immune responses to a panel of central nervous system antigens were assessed during the initial week and again at Day 90. Outcome was assessed using the modified Rankin Scale. Patients who developed an infection, especially pneumonia, in the 15 days after stroke were more likely to evidence a Th1(+) response to myelin basic protein and glial fibrillary acidic protein (P=0.019 and P=0.039, respectively) at 90 days after stroke. Further, more robust Th1 responses to myelin basic protein at 90 days were associated with a decreased likelihood of good outcome, even after adjusting for baseline stroke severity and patient age (OR, 0.477; 95% CI, 0.244 to 0.935; P=0.031). This study demonstrates that immune responses to brain antigens occur after stroke. Although these responses are likely to be an epiphenomenon of ischemic brain injury, the response to myelin basic protein appears to have clinical consequences. The potential role of postischemic autoimmune-mediated brain injury deserves further investigation.

Effects of estradiol on ischemic factor-induced astrocyte swelling and AQP4 protein abundance.

In the early hours of ischemic stroke, cerebral edema forms as Na, Cl, and water are secreted across the blood-brain barrier (BBB) and astrocytes swell. We have shown previously that ischemic factors, including hypoxia, aglycemia, and arginine vasopressin (AVP), stimulate BBB Na-K-Cl cotransporter (NKCC) and Na/H exchanger (NHE) activities and that inhibiting NKCC and/or NHE by intravenous bumetanide and/or HOE-642 reduces edema and infarct in a rat model of ischemic stroke. Estradiol also reduces edema and infarct in this model and abolishes ischemic factor stimulation of BBB NKCC and NHE. There is evidence that NKCC and NHE also participate in ischemia-induced swelling of astrocytes. However, little is known about estradiol effects on astrocyte cell volume. In this study, we evaluated the effects of AVP (100 nM), hypoxia (7.5% O(2)), aglycemia, hypoxia (2%)/aglycemia [oxygen glucose deprivation (OGD)], and estradiol (1-100 nM) on astrocyte cell volume using 3-O-methyl-d-[(3)H]glucose equilibration methods. We found that AVP, hypoxia, aglycemia, and OGD (30 min to 5 h) each significantly increased astrocyte cell volume, and that estradiol (30-180 min) abolished swelling induced by AVP or hypoxia, but not by aglycemia or OGD. Bumetanide and/or HOE-642 also abolished swelling induced by AVP but not aglycemia. Abundance of aquaporin-4, known to participate in ischemia-induced astrocyte swelling, was significantly reduced following 7-day but not 2- or 3-h estradiol exposures. Our findings suggest that hypoxia, aglycemia, and AVP each contribute to ischemia-induced astrocyte swelling, and that the edema-attenuating effects of estradiol include reduction of hypoxia- and AVP-induced astrocyte swelling and also reduction of aquaporin-4 abundance.

Matrix metalloproteinase-9 contributes to the increase of tau protein in serum during acute ischemic stroke

Previous studies indicate that tau protein, a marker of damage to neurons, is present in the serum of healthy patients at a concentration approximately 40 percent that of patients with ischemic stroke We assumed that increased serum activity of gelatinases (matrix metalloproteinase [MMP]-2 and MMP-9) can influence the level of tau protein in serum, probably due to disruption of the blood-brain barrier. We obtained blood sera from 31 patients admitted within the first 24 hours of ischemic stroke on days 1, 5 and 10, following the onset of stroke. Tau protein was detected in the serum of 12 patients (38.7 percent). The highest MMP-9 activity was recorded on day 5 (p < 0.05). Serum gelatinase activity did not differ between tau protein-positive or -negative individuals. However, a high degree of correlation between mean MMP-9 activity and the maximum tau protein level was observed for patients with detectable tau protein (r = 0.71, p = 0.009). Our study suggests that MMP-9 can increase the tau protein level in the sera of patients during acute ischemic stroke.

Trial of Insulin for Poststroke Hyperglycemia

The effect of glucose potassium insulin (GKI) infusion (compared to saline as control) within 24 hours of ischemic stroke was studied in patients (> 18 years old) with blood glucose >126mg/dl (7mmol/l) admitted to Southern General Hospital, Glasgow, Scotland.

Randomized, controlled trial of insulin for acute poststroke hyperglycemia

Poststroke hyperglycemia is common and is associated with increased risk of death and dependence, but appropriate management remains uncertain. Glucose potassium insulin (GKI) infusion did not benefit patients with moderate poststroke hyperglycemia in a recent trial. Using magnetic resonance imaging (MRI), previous studies identified a relationship between recruitment of ischemic tissue to the final infarct and hyperglycemia, possibly mediated by brain lactic acidosis. We undertook a randomized, placebo-controlled trial of GKI infusion in patients with blood glucose >126mg/dl (7mmol/l) within 24 hours of ischemic stroke. The primary endpoint was infarct growth on MRI between baseline and day 7. Brain lactate concentrations were measured with magnetic resonance spectroscopy. Forty patients were randomized, 15 to saline and 25 to GKI infusions of different durations. Capillary blood glucose concentrations were lowered significantly from 6 to 12 hours after GKI initiation. There was no significant difference on any measure of infarct growth between the GKI and saline groups. In a secondary analysis, GKI was associated with significantly greater infarct growth in patients with complete intracranial vessel occlusion compared with controls (p = 0.011 for group-vessel status interaction). Brain lactate levels increased in control subjects, but were significantly lower with GKI infusion. Predominantly asymptomatic hypoglycemia occurred in 76% of GKI-treated subjects. GKI infusion within 24 hours of stroke lowered blood glucose and attenuated an increase in brain lactate, but did not affect cerebral infarct growth. Exploratory analysis found that GKI infusion was associated with greater infarct growth in patients with persistent arterial occlusion, and with a high incidence of asymptomatic hypoglycemia.

Effect of Combined Aspirin and Extended-Release Dipyridamole Versus Clopidogrel on Functional Outcome and Recurrence in Acute, Mild Ischemic Stroke

Long-term antiplatelet therapy is effective at reducing recurrence after ischemic stroke. However, the relative safety and efficacy of combined aspirin-dipyridamole or clopidogrel are not known in patients with acute ischemic stroke. The factorial PRoFESS secondary prevention trial assessed antiplatelet and blood pressure-lowering strategies in 20,332 patients, 1360 of whom were randomized within 72 hours of ischemic stroke to combined aspirin (Asp; 25 mg BID) and extended-release dipyridamole (ER-DP; 200 mg BID, n=672) or clopidogrel (75 mg/d, n=688). The primary outcome for this post hoc subgroup analysis was functional outcome at 30 days; secondary outcomes included recurrence and death by 90 days. Analyses were adjusted for baseline prognostic variables and blood pressure treatment assignment. Patients were representative of the whole trial (age 67 years, National Institutes of Health Stroke Scale score 3, small-artery occlusion 59%), and baseline variables were similar between treatment groups. The mean time from stroke to recruitment was 58 hours. By 90 days, treatment was no longer being taken in 121 (18%) patients randomized to Asp/ER-DP and in 86 (12.5%) assigned to clopidogrel (P=0.006). Combined death or dependency (shift analysis of modified Rankin Scale score at day 30) did not differ between treatment groups (odds ratio [OR]=0.97; 95% CI, 0.79 to 1.19). Nonsignificant trends to reduced recurrence (OR=0.56; 95% CI, 0.26 to 1.18) and vascular events (OR=0.71; 95% CI, 0.36 to 1.37) were present with Asp/ER-DP. Rates of death, major bleeding, and serious adverse events did not differ between treatment groups. Treatment with combined Asp/ER-DP vs clopidogrel in 1360 patients with acute, mild ischemic stroke did not differ in terms of effects on functional outcome, recurrence, death, bleeding, or serious adverse events. Both treatments were practical to administer.

CITICOLIN IN THE TREATMENT OF STROKE AND VASCULAR COGNITIVE DISORDERS

Citicolin (ceraxon) is used as a neuroprotector in the treatment of acute stroke and vascular cognitive disorders. Experimental animal studies have demonstrated that citicolin reduces the extent of cerebral infarct and increases the degree of functional recovery. A few clinical trials have provided evidence for the efficacy of intravenous or oral citicolin used within the first 24 hours of ischemic stroke or cerebral hemorrhage in recovery of neurological functions. Citicolin is effective in memory and behavioral disorders in elderly patients with chronic cerebrovascular diseases. The use of citicolin has been found to be safe in stroke and vascular cognitive disorders

Fragmentation of the Classical Magnetic Resonance Mismatch “Penumbral” Pattern With Time

The classical mismatch pattern in the middle cerebral artery territory stroke on MR is defined by a central diffusion-weighted image core with surrounding mismatch tissue. Because of variable rates of tissue salvage, we hypothesized that this pattern may fragment over time and may be influenced by vessel patency, mismatch volume, and infarct core location. Patients were recruited with MR studies performed within 48 hours of ischemic stroke. Mismatch patterns based on diffusion-weighted/perfusion-weighted images were categorized as classical (majority of the diffusion-weighted image within the perfusion-weighted image lesion) or nonclassical (fragmented) patterns. The proportion of patterns was assessed with reference to time, vessel patency, mismatch volume, and infarct core location. Sixty-seven patients (33 classical [49.3%] and 34 nonclassical patterns [50.7%]) were studied within 48 hours (median age, 74.0 years). Compared to the nonclassical pattern, the classical pattern had a shorter time to MR (3.4 hours vs 10.4 hours; P=0.004) and a larger mismatch volume (62.0 mL vs 3.5 mL; P<0.0001). The positive predictors for the classical pattern were earlier time, vessel occlusion, superficial core location, and larger mismatch volume. The classical mismatch pattern may fragment with time. Over 48 hours the classical pattern is seen earlier after stroke onset, with higher rates of vessel occlusion and larger mismatch volumes.

Effect of Telmisartan on Functional Outcome, Recurrence, and Blood Pressure in Patients With Acute Mild Ischemic Stroke

High blood pressure (BP) is common in acute ischemic stroke and associated independently with a poor functional outcome. However, the management of BP acutely remains unclear because no large trials have been completed. The factorial PRoFESS secondary stroke prevention trial assessed BP-lowering and antiplatelet strategies in 20 332 patients; 1360 were enrolled within 72 hours of ischemic stroke, with telmisartan (angiotensin receptor antagonist, 80 mg/d, n=647) vs placebo (n=713). For this nonprespecified subgroup analysis, the primary outcome was functional outcome at 30 days; secondary outcomes included death, recurrence, and hemodynamic measures at up to 90 days. Analyses were adjusted for baseline prognostic variables and antiplatelet assignment. Patients were representative of the whole trial (age 67 years, male 65%, baseline BP 147/84 mm Hg, small artery disease 60%, NIHSS 3) and baseline variables were similar between treatment groups. The mean time from stroke to recruitment was 58 hours. Combined death or dependency (modified Rankin scale: OR, 1.03; 95% CI, 0.84-1.26; P=0.81; death: OR, 1.05; 95% CI, 0.27-4.04; and stroke recurrence: OR, 1.40; 95% CI, 0.68-2.89; P=0.36) did not differ between the treatment groups. In comparison with placebo, telmisartan lowered BP (141/82 vs 135/78 mm Hg, difference 6 to 7 mm Hg and 2 to 4 mm Hg; P<0.001), pulse pressure (3 to 4 mm Hg; P<0.002), and rate-pressure product (466 mm Hg.bpm; P=0.0004). Treatment with telmisartan in 1360 patients with acute mild ischemic stroke and mildly elevated BP appeared to be safe with no excess in adverse events, was not associated with a significant effect on functional dependency, death, or recurrence, and modestly lowered BP.

Negative fluid‐attenuated inversion recovery imaging identifies acute ischemic stroke at 3 hours or less

To evaluate the use of fluid-attenuated inversion recovery (FLAIR) imaging as surrogate marker of lesion age within the first 6 hours of ischemic stroke. e analyzed FLAIR and diffusion-weighted imaging (DWI) sequences performed within 6 hours of symptom onset in 120 consecutive patients with ischemic stroke with known symptom onset. The visibility of acute ischemic lesions on FLAIR images was judged in two steps (on FLAIR alone and with knowledge of DWI) and compared with DWI. egative FLAIR in the case of positive DWI allocated ischemic lesions to a time window 3 hours or less with a high specificity (0.93) and a high positive predictive value (0.94), whereas sensitivity (0.48) and negative predictive value (0.43) were low. Lesion visibility on FLAIR images alone (35.6%) and with knowledge of DWI (62.5%) was lower than on DWI (97.1%). The sensitivity of FLAIR increased with increasing time from symptom onset from 27.0/50.0% <or= 3 hours to 56.7/93.3% after 3 to 6 hours (FLAIR alone/with knowledge of DWI). Multivariate regression analysis spotted longer time from symptom onset and larger size of the ischemic lesion as independent predictors of lesion visibility on FLAIR images. "mismatch" between positive DWI and negative FLAIR allows the identification of patients that are highly likely to be within the 3-hour time window. Within the first 6 hours of stroke, the sensitivity of FLAIR sequences for acute ischemic lesions increases with time from symptom onset elapsing, approximating 100% after 3 to 6 hours.

Cerebral microvascular endothelial cell Na/H exchange: evidence for the presence of NHE1 and NHE2 isoforms and regulation by arginine vasopressin

Blood-brain barrier (BBB) Na transporters are essential for brain water and electrolyte homeostasis. However, they also contribute to edema formation during the early hours of ischemic stroke by increased transport of Na from blood into brain across an intact BBB. We previously showed that a luminal BBB Na-K-Cl cotransporter is stimulated by hypoxia, aglycemia, and AVP and that inhibition of the cotransporter by intravenous bumetanide significantly reduces edema and infarct in the rat middle cerebral artery occlusion (MCAO) model of stroke. More recently, we found evidence that intravenous cariporide (HOE-642), a highly potent Na/H exchange inhibitor, also reduces brain edema after MCAO. The present study was conducted to investigate which Na/H exchange protein isoforms are present in BBB endothelial cells and to evaluate the effects of ischemic factors on BBB Na/H exchange activity. Western blot analysis of bovine cerebral microvascular endothelial cells (CMEC) and immunoelectron microscopy of perfusion-fixed rat brain revealed that Na/H exchanger isoforms 1 and 2 (NHE1 and NHE2) are present in BBB endothelial cells. Using microspectrofluorometry and the pH-sensitive dye BCECF, we found that hypoxia (2% O(2), 30 min), aglycemia (30 min), and AVP (1-200 nM, 5 min) significantly increased CMEC Na/H exchange activity, assessed as Na-dependent, HOE-642-sensitive H(+) flux. We found that AVP stimulation of CMEC Na/H exchange activity is dependent on intracellular Ca concentration and is blocked by V(1), but not V(2), vasopressin receptor antagonists. Our findings support the hypothesis that a BBB Na/H exchanger, possibly NHE1 and/or NHE2, is stimulated during ischemia to participate in cerebral edema formation.

Bumetanide and HOE642 administered after initiation of rat middle cerebral artery occlusion effectively reduce rat brain Na uptake and infarct

Increased brain Na uptake across an intact blood‐brain barrier (BBB) contributes to cerebral edema formation in the early hours of ischemic stroke. We have shown previously that a luminal BBB Na‐K‐Cl cotransporter and Na/H exchanger are stimulated by ischemic factors and that both edema and infarct induced by middle cerebral artery occlusion (MCAO) are reduced by i.v. bumetanide or HOE642, inhibitors of the cotransporter and exchanger, respectively. The present study was conducted to determine whether bumetanide and HOE642 reduce the brain Na uptake that underlies edema in ischemic stroke and further, whether they are effective when given after the onset of ischemia. Rats were given bumetanide (30 mg/kg), HOE642 (30 mg/kg) or vehicle i.v. 20 min before, or 1 or 2 hr after initiation of left MCAO. Localized 23Na magnetic resonance spectroscopy with the shift reagent DyTTHA was used to assess total and extravascular brain [Na] in selected regions of interest during up to 5 hr of MCAO. The ipsilateral/contralateral brain ratios of both total [Na] and extravascular [Na] increased linearly following induction of ischemia. Bumetanide and HOE642 significantly reduced brain Na uptake and infarct when given before or after the start of MCAO. Our findings suggest that inhibition of the Na‐K‐Cl cotransporter and Na/H exchanger, even 2 hr after the start of ischemia, effectively reduces brain Na uptake and infarct.Supported by NINDS

Changes in NAA and lactate following ischemic stroke

Although much tissue damage may occur within the first few hours of ischemic stroke, the duration of tissue injury is not well defined. We assessed the temporal pattern of neuronal loss and ischemia after ischemic stroke using magnetic resonance spectroscopic imaging (MRSI) and diffusion-weighted imaging (DWI). We measured N-acetylaspartate (NAA) and lactate in 51 patients with acute ischemic stroke at five time points, from admission to 3 months, in voxels classified as normal, possibly or definitely abnormal (ischemic) according to the appearance of the stroke lesion on the admission DWI. We compared changes in NAA and lactate in different voxel classes using linear mixed models. NAA was significantly reduced from admission in definitely and possibly abnormal (p < 0.01) compared to contralateral normal voxels, reaching a nadir by 2 weeks and remaining reduced at 3 months. Lactate was significantly increased in definitely and possibly abnormal voxels (p < 0.01) during the first 5 days, falling to normal at 2 weeks, rising again later in these voxels. The progressive fall in N-acetylaspartate suggests that some additional neuronal death may continue beyond the first few hours for up to 2 weeks or longer. The mechanism is unclear but, if correct, then it is possible that interventions to limit this ongoing subacute tissue damage might add to the benefit of hyperacute treatment, making further improvements in outcome possible.

Gender differences in unilateral spatial neglect within 24 hours of ischemic stroke

Hemispatial neglect is a common and disabling consequence of stroke. Previous reports examining the relationship between gender and the incidence of unilateral spatial neglect (USN) have included either a large numbers of patients with few neglect tests or small numbers of patients with multiple tests. To determine if USN was more common and/or severe in men or women, we examined a large group of patients (312 right-handed) within 24 hours of acute right hemisphere ischemic stroke. Multiple spatial neglect tasks were used to increase the sensitivity of neglect detection. No differences based upon gender were observed for the prevalence, severity, or a combined task measure of USN.

Management of hypertension in the setting of acute ischemic stroke

The optimal management of blood pressure in the first 24 hours of ischemic stroke remains a controversial topic. Most patients are hypertensive at presentation and subsequently experience a spontaneous decline in blood pressure. Decreasing penumbral blood flow and exacerbating vasogenic edema are significant concerns in whether to treat blood pressure elevations. Although an initially elevated blood pressure has been associated with poor outcome, attempts to acutely lower blood pressure are also associated with worsened outcomes. Thus, the current approach in acute ischemic stroke is permissive hypertension, in which antihypertensive treatment is warranted in patients with systolic blood pressure greater than 220 mm Hg, receiving thrombolytic therapy, or with concomitant medical issues. The use of predictable and titratable medications that judiciously reduce (approximately 10% to 15%) the initial presenting mean arterial pressure is recommended in these situations. Future study must define optimal blood pressure goals, likely on an individual basis.

QEEG Prognostic Value in Acute Stroke

The objective of our study is to determine the predictive value of QEEG in patients suffering from an acute ischemic cerebral stroke. Twenty-eight patients were studied within the first 72 hours of clinical evolution of middle cerebral artery territory ischemic stroke. Thirty-seven QEEG recordings were obtained: 13 in the first 24 hours after cerebral stroke onset, 9 between 24-48 hours and 15 between 48-72 hours. Absolute Energies (AE) were the QEEG selected variables for statistical analysis: first, AE Z values were calculated using the Cuban QEEG norms, then the maximum and minimum AE Z values were selected within each frequency band and total power. The medians of the five neighboring Z values were also chosen. Regression models were estimated using the RANKIN scores as dependent variables and the selected QEEG variables as independent, then outcome predictions at hospital discharge and 3 months later were calculated. Percentages of concordance and errors between the estimated and real outcome scores were obtained. Alpha and theta AE were the best predictor for short-term outcome and delta AE for long-term outcome. We conclude that QEEG performed within the first 72 hours of ischemic stroke might be a powerful tool predicting short- and long-term outcome.