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The aim of this study was to investigate the relationship between the remaining corticospinal tract (CST) as determined by diffusion tensor imaging (DTI) and 6-month motor outcome in patients with pontine infarct. Ratios of fractional anisotropy (FA), fiber number (FN), and CST area were calculated, and the FN ratio and CST area ratio showed significant correlation with all 6-month motor outcome. Thus, the remaining CST in the pons measured using DTI at early stage of stroke could predict motor outcome in patients with pontine infarct. [ABSTRACT FROM PUBLISHER]

Sleep deprivation is associated with increased risk of myocardial infarction. However, it is unknown whether the effects of sleep deprivation are limited to increasing the likelihood of experiencing a myocardial infarction or if sleep deprivation also increases the extent of myocardial injury. In this study, rats were deprived of paradoxical sleep for 96 h using the platform-over-water method. Control rats were subjected to the same condition except the control platform was large enough for the rats to sleep. Hearts from sleep deprived and control rats were subjected to 20 min ischemia on a Langendorff isolated heart system. Infarct size and post ischemic recovery of contractile function were unaffected by sleep deprivation in male hearts. In contrast, hearts from sleep-deprived females exhibited significantly larger infarcts than hearts from control females. Post ischemic recovery of rate pressure product and + dP/dT were significantly attenuated by sleep deprivation in female hearts, and post ischemic recovery of end diastolic pressure was significantly elevated in hearts from sleep deprived females compared to control females, indicating that post ischemic recovery of both systolic and diastolic function were worsened by sleep deprivation. These data provide evidence that sleep deprivation increases the extent of ischemia-induced injury in a sex-dependent manner. [ABSTRACT FROM PUBLISHER]

Objectives: It has been suggested that metalloproteinase-9 (MMP-9) could predict the onset of cerebral vasospasm after subarachnoidal haemorrhage (SAH). The aim of this study was to analyse, in patients with SAH, the difference between patients with MRI ischaemic infarcts and patients without, and to investigate the role of metalloproteases as a prognostic factor for ischaemic infarcts. Methods: Sixty eight consecutive patients with SAH and diffusion-weighted magnetic resonance imaging (DWI-MRI) done 3 weeks after SAH. We define two groups, with and without DWI-MRI infarcts. Blood samples were taken at entry, 3 days and 1 week MMP-9 was determined through ELISA method. Results: Forty per cent were male, with a mean age of 54± 14 years. Twenty five patients, 36.8%, had DWIMRI infarcts; in patients with MRI infarcts, SAH was more severe (Fisher=4 52 vs 25.6%, P=0.037), with more morbi-mortality (Rankin>3 48 vs 18.6%, P=0.014), and more symptomatic vasospasm (28 vs 7%, P=.031). Levels of MMP-9 were higher than controls, but there were no significant differences between patients with and without infarcts (first determination no infarcts 39.40 ng/ml± 35.40 vs infarcts 49.75 ng/ml± 34.54, P>0.005, 3 days no infarcts 72.10 ng/ml± 70.95 vs infarcts 62.28± 33.84, P>0.005, 1 week no infarcts 148.48 ng/ml± 142.73 vs infarcts 91.51 ng/ml± 41.20, P>0.005). Conclusion: Thirty eight percent in a well-studied series of patients with SAH have DWI-MRI infarcts; the infarcts were associated to SAH severity, SAH outcome and symptomatic vasospasm. Metalloproteinase- 9 was higher in SAH patients than in controls, but it could not discriminate the infarct patients. [ABSTRACT FROM AUTHOR]

Object: Intracarotid cold saline infusion (ICSI) protects against ischemic stroke not only due to the resulting hypothermia, but also as a result of the cerebral artery flushing. To assess the relative benefit of hypothermia and cerebral artery flushing in neuroprotection, hypothermic and normothermic saline infusions were administrated over a serial time points after the initiation of reperfusion in a rat ischemia model. Methods: Ischemic strokes were induced in Sprague-Dawley rats (n=115) by occluding the middle cerebral artery for 2 hours using an intraluminal filament. In the hypothermic groups, the brain temperature was lowered to 33-34uC for 20 minutes by ICSI at three time points (0, 1, and 2 hours) after reperfusion. Correspondingly, in the normothermic groups, the brain temperature was maintained at normal levels during intracarotid normothermic saline infusion (INSI) for 20 minutes at the same time points. After 48-hour reperfusion, infarct sizes and brain water contents were determined using 2,3,5-triphenyltetrazolium chloride (TTC) staining and the dry-wet weight method, respectively. Levels of neuron-specific enolase (NSE), S100beta, and matrix metalloproteinase 9 (MMP9) in the serum were measured by enzyme-linked immunoassay (ELISA). Neurological deficits were also evaluated. Results: Immediate infusion after the onset of reperfusion (0 hour) did not result in significant difference for reductions of infarct sizes, neurological deficits or S100beta serum levels between ICSI and INSI groups, compared with the non-infusion group. However, brain water content and NSE serum level were significantly lower in the ICSI group than the non-infusion group. When the infusions were started 1 hour after reperfusion, both ICSI and INSI infusions still reduced the infarct sizes, but only ICSI significantly decreased the brain water content, neurological deficits and S100beta serum level. All therapeutic effects of INSI disappeared when infusions were started 2 hours after reperfusion, whereas infarct size, neurological deficits and S100beta serum level were still reduced significantly in ICSI group, compared with the non-infusion group. Conclusions: The neuroprotection of hypothermia and cerebral artery flushing induced by selective carotid infusion after ischemia weakens as the length of time between the reperfusion and infusion increases. The therapeutic time window of brain hypothermia induced by cold saline infusion is broader than cerebral artery flushing induced by normothermic saline infusion. [ABSTRACT FROM AUTHOR]

Objective and importance: Recent works on extradural cortical stimulation have been successful in improving neurological recovery in chronic stroke patients. On the other hand, single perirolandic stimulations are often associated with disappointing results. Clinical presentation: We report two cases of chronic stroke in which the magnitude of infarct was too large to be improved with single perirolandic stimulation. Patient 1 had severe hemiplegia associated with large cortical infarct in the right frontoparietal area. The patient could neither stand independently or walk. Patient 2 had hemiplegia and aphasia due to cortical infarct in the left middle cerebral artery territory. Both patients had intensive rehabilitative training for more than 6 months with no beneficial results. Intervention: Two paddle electrodes covering frontal and parietal area were implanted, followed by dual cortical stimulation with concurrent rehabilitative training in patient 1. After 6 months of stimulation, the patient could walk with a good posture. Two paddle electrodes were implanted to cover pre-motor and motor cortex in patient 2. After similar treatment, the motor function was markedly improved. Conclusion: Dual cortex stimulation, which acts on more diffuse areas or functionally related areas, is beneficial to promote the motor recovery in chronic stroke patients with large infarcts. [ABSTRACT FROM AUTHOR]

Objective: The neuroprotective effect of hypothermia has long been recognized. The aim of this work was to compare the neuroprotective effect of systemic, head and local vascular cooling hypothermia procedures in ischemic rats. Methods: Stroke in Sprague–Dawley rats (n=64) was induced by a 3 hour right middle cerebral artery occlusion using an intraluminal filament. Before reperfusion, ischemic animals (n=16 in each group) received hypothermia (systemic, head or local vascular) or no treatment. Brain temperature, infarction volume (n=8 in each group) and functional outcome (n=8 in each group) were compared. Results: Regarding brain temperature, vascular cooling significantly reduced the temperature of ischemic territory in cortex from 37·2 ± 0·1 to 33·4 ± 0·4°C and in striatum from 37·5 ± 0·2 to 33·9 ± 0·4°C within 5 minutes. This hypothermic condition remained for up to 60 minutes after reperfusion. However, systemic cooling reduced brain temperature at a similar level for six times longer. In the head cooling group, the target temperature was reached in 15 minutes, but returned to normal within 5 minutes. Although all hypothermia procedures induced neuroprotection, ischemic rats with vascular cooling showed significantly (p<0·001) better neuroprotection with 10·7 ± 2·6% infarction, compared to 54·2 ± 1·9% (no treatment), 37·1 ± 1·0% (head cooling) and 29·1 ± 3·4% (systemic cooling). Significantly (p<0·001) better effects on motor function were also detected in vascular cooling groups at 14 and 28 days. Conclusion: Vascular cooling appears to be the most effective in reducing infarct volume and improving functional outcome than the other two hypothermia methods in a rat ischemia/reperfusion model. [ABSTRACT FROM AUTHOR]

Objective. To compare pathological findings of placentas from term and preterm pregnancies complicated by intrauterine fetal death (IUFD). Study design. A retrospective cohort study was conducted including deliveries complicated by IUFD. A comparison was made between placentas from term and preterm (<37 weeks' gestation) pregnancies complicated by IUFD. A second analysis was undertaken comparing IUFD placentas delivered before and after 34 weeks' gestation. Uteroplacental insufficiency was defined when one or more of the following pathological features were found: placental infarct, poor vascularity of the chorionic villi, intravascular thrombi and vascular occlusion. Results. During the study period, 849 placentas of IUFD were examined. Gross and microscopic pathological finding were noted. When comparing gross and microscopic findings in term and preterm (<37 weeks) IUFD placentas, higher rates of calcifications, tissue congestion and cellular metaplasia were found in term vs. preterm placentas. Significantly increased rates of poor tissue vascularity, placental vascular occlusion and uteroplacental insufficiency were demonstrated in preterm IUFD placentas. When comparing pathological findings in IUFD placentas delivered before and after 34 weeks' gestation, higher rates of abnormal cord insertion, calcifications, tissue congestion, infarcts and intravascular thrombi as well as poor tissue vascularity and placental vascular occlusion were demonstrated in IUFD placentas delivered before 34 weeks. Regardless of gestational age at the time of IUFD in more than 90% of placentas vascular wall thickening was found. A third of both term and preterm placentas demonstrated histological chorioamionitis. Conclusions. A vast majority of IUFD placentas reveal numerous pathological findings that reflect uteroplacental insufficiency and abnormal blood supply. Different characteristics were noted in term and preterm placentas of pregnancies complicated by IUFD. Better definition of causes and associated placental pathological findings of IUFD might aid clinicians in counseling such patients regarding the reason and risk of recurrence in subsequent pregnancies. [ABSTRACT FROM AUTHOR]

Objectives: The aims of this study were to determine the effects of intra-arterial local hypothermia on infarct volume in rats with different durations of ischemia and to determine whether hypothermia can prolong the therapeutic time window compared with reperfusion without hypothermia. Methods: Adult male Sprague-Dawley rats weighing 260–300 g were divided into control group (permanent MCA occlusion), normothermia groups (NT groups) and hypothermia groups (HT groups). NT groups included rats induced with blood reperfusion for 1.5, 2, 2.5 or 3 hour ischemia. In the HT groups with ischemia of 1.5, 2, 2.5 or 3 hours, 6 ml 20°C normal saline solution was flushed at a speed of 0.6 ml/min, beginning 10 minutes before blood reperfusion. The infarct volumes of brains stained by TTC were observed 48 hours later. Brain temperature, blood flow and neurological scores were also recorded during this procedure. Results: In the 1.5, 2, 2.5 and 3 hour ischemic groups, cold saline (20°C infusion via the MCA) rapidly reduced the temperature of the MCA-supplied ischemic territory in the cortex from 37.0–37.1 to 32.8–33.2°C and in the striatum from 37.3–37.5 to 33.2–33.3°C. In NT groups, the average total infarct volumes of 1.5 and 2 hour ischemia (29.80 ± 2.20 and 34.29 ± 2.14%, respectively) were significantly less than that of the control group (48.41 ± 5.82%), but the average total infarct volumes of the 2.5 and 3 hour ischemia groups (47.31 ± 4.72 and 50.17 ± 8.08%, respectively) did not change. Compared with the ischemia groups without local saline infusion, the average total infarct volumes of 1.5, 2 and 2.5 hours with local saline infusion to the ischemic territory (16.79 ± 2.51, 23.09 ± 4.63% and 25.19 ± 7.82%, respectively) decreased significantly, but the average total infarct volume of 3 hour ischemia with local saline infusion (43.30 ± 2.62%) was not different. Conclusion: Local cold saline infusion to the ischemic territory before reperfusion can lead to mild hypothermia of the ischemic territory and can prolong the therapeutic time window of reperfusion from 2 to 2.5 hours. Refinements of the cooling process, optimal target temperature, duration of the therapy and most importantly, clinical efficacy, require further study. [ABSTRACT FROM AUTHOR]

Purpose: In ischemic myocardium systolic strain is reduced and followed by a deformation after systole, the so-called post-systolic shortening. The presence of post systolic shortening is therefore considered a marker of viability even though its mechanism remains unclear. The hypothesis was tested whether post-systolic shortening might be a passive recoil phenomenon and therefore not uniquely associated with viability. Methods: Five patients with a history of myo-cardial infarctions and fully transmural scars in late enhancement imaging and five age-matched healthy volunteers underwent a tagging study to analyze systolic and post-systolic deformation in transmurally infarcted and contra-lateral non-infarcted myocardium. From CSPAMM myocardial tagging data, mid-wall circumferential fiber shortening, radial displacement, and rotation parameters were semi-automatically extracted by harmonic phase (HARP). Results: In transmurally infarcted myocardium, a post systolic shortening of 6.2 ± 1.8% was present occurring in early diastole (time to maximum circumferential fiber shortening increased versus both, contra-lateral myocardium and corresponding sectors in healthy volunteers, p < 0.01). Maximum radial displacement was decreased in scar tissue (p < 0.001 versus contra-lateral), but time to maximum radial displacement did not differ. Rotation did not discriminate between infarcted and non-infarcted myocardium. Conclusions: The pure finding of post-systolic shortening is not sufficient for the diagnosis of residual myocardial viability. Post-systolic shortening may be explained in part by passive recoil, which releases energy stored in the scar tissue during systolic intra-ventricular unloading. Circumferential fiber shortening appears best suited for characterization of regional deformation, whereas radial displacement and rotation are more dependent on tethering effects, and thus, are more likely to reflect global chamber mechanics. [ABSTRACT FROM AUTHOR]

Increasing evidence indicates that physical activity reduces brain damage after stroke. The purpose of this study was to determine whether exercise-induced neuroprotection is associated with improved brain integrity in stroke. Adult male Sprague–Dawley rats (3 months old, n=38) exercised on a treadmill, which required repetitive locomotor movement, for 30 minutes each day for 3 weeks. Then, using an intraluminal filament, stroke was induced by either 2 hours middle cerebral artery (MCA) occlusion followed by 24 or 48 hours of reperfusion. Brain damage was determined by evaluating brain infarction and brain edema, as well as ultrastructural alteration in endothelial–matrix–astrocyte interfaces. Pre-ischemic motor exercise significantly (p<0.01) reduced infarct volume in the frontoparietal cortex and the dorsolateral striatum by 79%. By comparing the percentage difference in brain volume between the right (stroke site) and left hemispheres, we demonstrated a significant (p<0.01) reduction in brain edema associated with reduced infarct volume in a 3 week exercise group (Group 1, n=10) and a 3 week exercise plus 3 week rest group (Group 2, n=10). Edema in cortex and striatum was 19 ± 4% without exercise pre-conditioning (n=10), in contrast to 5 ± 3% (Group 1) or 6 ± 4% (Group 2). The thickness of the basal lamina was enhanced by exercise. In ischemic rats without pre-exercise, alterations in microvessel ultrastructure with decreased luminal area, parenchymal edema and swollen astrocyte end-feet, as well as an abnormally thin basal lamina were observed. In contrast, exercise pre-conditioning significantly reduced the ischemic alterations, decreasing brain edema and increasing basal lamina thickness. This study suggests that exercise pre-conditioning reduces brain injury by decreasing cerebral permeability and enhancing brain integrity after stroke. This exercise-induced endogenous neuroprotection could be an effective strategy to ameliorate ischemic brain injury from stroke. [ABSTRACT FROM AUTHOR]

Other than from the thalamus and sensory cortex, episodic pain is an extremely rare neurological manifestation in the central compartment. This study reports a middle-aged man who experienced an acute onset of episodic oscillatory burning pain restricted to the cheiro-oral region, who was found to have a singular infarct at the left tegmental pons. A close relationship between his pain attack and an elevation of arterial blood pressure was clearly observed. Blood adenohypophyseal hormones and electroencephalogram did not reveal an abnormality in the ictus. Neuroimaging and clinical studies did not support involvement of the thalamus, periaqueductal gray matter, hypothalamus or regional structure. Therefore, episodic pain may be an isolated manifestation with a pontine lesion. A relapsing expansion of focal cerebral oedema with fluid retention may have corresponded to the oscillation of his sensory deficit. This accumulating, devastating calamity by a repetitive and paroxysmal offense after a blood–brain barrier breakdown should be cautiously reviewed. [ABSTRACT FROM AUTHOR]

An 11-year-old girl presented with Plasmodium vivax malaria complicated by shock and acute renal failure. The diagnosis of malaria was based on demonstration of trophozoites of P. vivax in the peripheral blood smear and a positive rapid malarial antigen test for P. vivax but negative for P. falciparum. She responded to parenteral artesunate and supportive care. During the course of her infection, she developed pain in her left hypochondrium. Ultrasonography showed multiple hypo-echoic lesions in the spleen and CT scan revealed multiple splenic infarcts. Management was restricted to close clinical monitoring and analgesia. We consider that this is the first report of splenic infarct complicating the course of childhood P. vivax malaria in the English literature. Physicians should suspect and investigate for this rare complication if a patient with malaria complains of left upper quadrant abdominal pain, pleuritic left lower chest pain and/or enlarging tender splenomegaly during the course of malaria infection. [ABSTRACT FROM AUTHOR]

We report an artefactual middle cerebral artery territory infarct on CT scan. This anomaly is suggested by the discrepancy between the clinical and radiological findings. Awareness of this possibility may avoid unnecessary further investigation or treatment. [ABSTRACT FROM AUTHOR]