Lipoprotein-associated phospholipase A2 Activity Levels is Associated with Artery to Artery Embolism in Symptomatic Intracranial Atherosclerotic Disease.

BACKGROUND: Lipoprotein-associated phospholipase A2 activity (Lp-PLA2-A) is a pivotal enzyme involved in the inflammatory process and atherosclerotic plaque vulnerability. This study aimed to investigate the potential of Lp-PLA2-A as a biomarker for reflecting artery-to-artery embolism (AAE), a critical mechanism with high risk of stroke recurrence in symptomatic intracranial atherosclerotic disease (sICAD). METHODS: The current analysis included a cohort of 1,908 patients with sICAD and baseline levels of Lp-PLA2-A from the Third China National Stroke Registry (CNSR-III). The baseline Lp-PLA2-A levels were quantified centrally using an automatic enzyme assay system. Diagnosis of sICAD was made by experienced stroke neurologists based on the presence of a cerebral infarction within the territory of a stenotic (>50%) or occluded artery, or when clinical symptoms were consistent with the diagnosis. Infarct lesions affecting the cortex serve as imaging biomarkers for stroke mechanism involving AAE.The relationship between baseline Lp-PLA2-A quartile levels and the presence of cortical infarction was analyzed using multivariate logistic regression. RESULTS: Compared to patients in the first Lp-PLA2-A quartile, those in the second, third and fourth quartiles demonstrated a significantly higher proportion of AAE. The proportion of patients with cortical infarction increased with rising Lp-PLA2-A quartiles, observed at 39.3%, 47.1%, 47.4%, and 50.7% for the first, second, third and fourth quartiles respectively (P for trend=0.004). Compared with the first quartile, the odds ratios (ORs) were 1.38 (95% CI = 1.06-1.79) for the second, 1.33 (95% CI = 1.02-1.72) for the third quartile and 1.48 (95% CI = 1.14-1.92) for the fourth quartile. The association between higher Lp-PLA2-A and increased proportion of cortical infarction was also present in the subgroups defined by age <65 years, male, and high-sensitivity C-reactive protein ≥2 mg/L. In sensitivity analyses, the positive correlation between Lp-PLA2-A levels and proportion of cortical infarction remained consistent. CONCLUSIONS: This research highlights the significance of Lp-PLA2-A as a biomarker for reflecting stroke mechanism in sICAD. Additional studies are warranted to explore the potential of targeting Lp-PLA2-associated inflammatory pathways as a pivotal approach in arresting the advancement of intracranial atherosclerotic stenosis and reducing the incidence of embolic strokes.

Preclinical examination of early-onset thalamic-cortical seizures after hemispheric stroke.

OBJECTIVE: Ischemic stroke is one of the main causes of death and disability worldwide and currently has limited treatment options. Electroencephalography (EEG) signals are significantly affected in stroke patients during the acute stage. In this study, we preclinically characterized the brain electrical rhythms and seizure activity during the hyperacute and late acute phases in a hemispheric stroke model with no reperfusion. METHODS: EEG signals and seizures were studied in a model of hemispheric infarction induced by permanent occlusion of the middle cerebral artery (pMCAO), which mimics the clinical condition of stroke patients with permanent ischemia. Electrical brain activity was also examined using a photothrombotic (PT) stroke model. In the PT model, we induced a similar (PT group-1) or smaller (PT group-2) cortical lesion than in the pMCAO model. For all models, we used a nonconsanguineous mouse strain that mimics human diversity and genetic variation. RESULTS: The pMCAO hemispheric stroke model exhibited thalamic-origin nonconvulsive seizures during the hyperacute stage that propagated to the thalamus and cortex. The seizures were also accompanied by progressive slowing of the EEG signal during the acute phase, with elevated delta/theta, delta/alpha, and delta/beta ratios. Cortical seizures were also confirmed in the PT stroke model of similar lesions as in the pMCAO model, but not in the PT model of smaller injuries. SIGNIFICANCE: In the clinically relevant pMCAO model, poststroke seizures and EEG abnormalities were inferred from recordings of the contralateral hemisphere (noninfarcted hemisphere), emphasizing the reciprocity of interhemispheric connections and that injuries affecting one hemisphere had consequences for the other. Our results recapitulate many of the EEG signal hallmarks seen in stroke patients, thereby validating this specific mouse model for the examination of the mechanistic aspects of brain function and for the exploration of the reversion or suppression of EEG abnormalities in response to neuroprotective and anti-epileptic therapies.

Hemichorea secondary to isolated temporal infarction with severe middle cerebral artery stenosis: a case report and review of literature.

BACKGROUND: Hemichorea typically results from a contralateral subthalamic nuclei (STN) lesion, although it has been reported in the cortex in a minority of cases. However, to our best knowledge, there are no documented cases in literature of hemichorea occurring as a secondary condition to an isolated temporal stroke. CASE PRESENTATION: We present a case of an elderly female who sustained a sudden onset of hemichorea in her right extremities, predominantly in the distal region, lasting over a period of two days. Brain diffuse weighted image (DWI) demonstrated a high signal in the temporal region, while magnetic resonance angiography (MRA) revealed severe stenosis of the middle cerebral artery. During the symptomatic phase, computed tomography perfusion (CTP) revealed delayed perfusion in the left middle cerebral artery territory, characterized by the time-to-peak (TTP) measure. Based on the results of her medical history and laboratory tests, we were able to rule out the possibility of infectious, toxic, or metabolic encephalopathy. Her symptoms gradually improved with antithrombotic and symptomatic treatment. CONCLUSIONS: It is important to recognize and consider acute onset hemichorea as an initial symptom of stroke to avoid misdiagnosis and delays in appropriate treatment. Further research on temporal lesion that lead to hemichorea is warranted to gain a better understanding of the underlying mechanisms.

Hemichorea in a patient with ipsilateral cortical infarction: a case report.

BACKGROUND: Hemichorea is usually caused by contralateral deep structures of brain. It rarely results from acute cortical ischemic stroke and that caused by ipsilateral brain lesions is even rarer. CASE PRESENTATION: A 64-year-old female presented with acute obtuseness and left-sided hemichorea. She had a history of right frontal lobe surgery and radiotherapy due to brain metastasis from lung cancer 8 years ago. MRI revealed acute left frontal lobe infarction in addition to an old right frontal lobe lesion. 18FDG PET-CT showed hypometabolism in the left frontal lobe and hypermetabolism in the right basal ganglia region and central sulcus. The choreatic movement remitted after antipsychotic treatment. CONCLUSION: The mechanism of hemichorea after ipsilateral cortical infarction is poorly understood. We assume both previous contralateral brain lesion and recent ipsilateral ischemic stroke contributed to the strange manifestation in this case.

Spontaneous Neuronal Plasticity in the Contralateral Motor Cortex and Corticospinal Tract after Focal Cortical Infarction in Hypertensive Rats.

OBJECTIVES: In this study, we investigated the spontaneous neural plasticity on the contralateral side in hypertensive rats, including the expression of nerve growth factors (synaptophysin [SYN] and growth-associated protein 43 [GAP-43]), and the association between nerve fiber sprouting and redistribution, and the recovery of motor functions following sensorimotor cortical infarction. METHODS: Initially, Sprague-Dawley rats were induced with renal hypertension by the bilateral renal arteries clips method. Further, they were induced with cerebral ischemia by the middle cerebral artery electrocoagulation method; 70 male rats completed the study. We compared the changes in the corticospinal tract (CST) and the expressions of SYN and GAP-43 on the contralateral side in rats with cerebral infarction using immunohistochemical staining, western blot, and biotinylated dextran amine (BDA) tracing analyses. The recovery of motor function in rats after cortical infarction was evaluated by the foot-fault and beam-walk tests. RESULTS: The motor behavior tests revealed that the motor function of rats could recover to various degrees after focal cortical infarction. Compared with the sham-operated group, the SYN and GAP-43 levels increased in the motor cortex of the opposite hemisphere within 28 days after middle cerebral artery occlusion (MCAO). The increase in SYN and GAP-43 expressions presented differently in layers Ⅱ, Ⅲ, and Ⅴ. The amount of BDA-positive fibers also increased significantly in the denervated cervical spinal gray matter on day 56 post-MCAO. CONCLUSIONS: The increases in SYN and GAP-43 on the contralateral side of the motor cortex could promote CST sprouting and rewiring in the spinal cord gray matter and also spontaneous motor function recovery after cortical infarction.

Visualization of Regional Cerebral Blood Flow Dynamics during Cortical Venous Occlusion using Laser Speckle Contrast Imaging in a Rat Model.

BACKGROUND: Cerebral venous ischemia (CVI) is a rare but potentially significant complication of neurosurgical procedures. However, it is still unclear how cerebral venous occlusion (VO) affects regional cerebral blood flow (rCBF) dynamics. To elucidate its pathophysiology in detail, we examined the real-time perfusion dynamics during adjacent vein occlusions using laser speckle contrast imaging (LSCI) in a rat 2-vein occlusion model. METHODS: Two cortical veins were occluded photochemically using rose Bengal dye in 6 male Wistar rats; rCBF was measured in real time with an LSCI before and after VO. Regions of interest were defined between the 2 veins (A) and on the opposite side of the first occluded vein (B) on semi-quantitative pseudocolor images for off-line analysis. Histopathologic evaluation was performed 3 days after the procedure to assess the extent of infarction. RESULTS: LSCI revealed a stepwise reduction in CBF, with a sudden decrease just after the first vein occlusion (~20%) and a further decrease after the second (~30%). Significant differences were observed between rCBF dynamics within regions of interest A and B (P = .0004). All rats exhibited infarcts in the superficial cerebral cortex histopathologically. CONCLUSIONS: This is the first report of LSCI specifically applied to the study of CVI. The extensive real-time measurement with high temporal and spatial resolution revealed the stepwise reduction in rCBF during sequential VO and the ensuing infarcts.

Dorsal dentate gyrus mediated enriched environment-induced anxiolytic and antidepressant effects in cortical infarcted mice.

Anxiety and depression are the most common mental health disorders worldwide, each affecting around 30% stroke survivors. These complications not only affect the functional recovery and quality of life in stroke patients, but also are distressing for caregivers. However, effective treatments are still lacking. Enriched environment (EE), characterized with novel and multi-dimensional stimulation, has been reported to exert therapeutic effects on physical and cognitive function. In addition, EE also had potential positive effects on emotional disorders after ischemic stroke; however, the underling mechanisms have not been well elucidated. This study aimed to explore the effectiveness of EE on emotional disorders after cerebral ischemia and its underling mechanism. Sensorimotor cortical infarction was induced by photothrombosis with stable infarct location and volume, resulting in motor dysfunction, anxiety and depression-like behaviors in mice, with decreased ALFF and ReHo values and decreased c-fos expression in the infarction area and adjacent regions. Seven days' EE treatment significantly improved motor function of contralateral forelimb and exhibited anxiolytic and antidepressant effects in infarcted mice. Compared to the mice housing in a standard environment, those subjected to acute EE stimulation had significantly increased ALFF and ReHo values in the bilateral somatosensory cortex (S1, S2), dorsal dentate gyrus (dDG), dorsal CA1 of hippocampus (dCA1), lateral habenular nucleus (LHb), periaqueductal gray (PAG), ipsilateral primary motor cortex (M1), retrosplenial cortex (RSC), parietal association cortex (PtA), dorsal CA3 of hippocampus (dCA3), claustrum (Cl), ventral pallidum (VP), amygdala (Amy), and contralateral auditory cortex (Au). Some of, but not all, the ipsilateral brain regions mentioned above showed accompanying increases in c-fos expression with the most significant changes in the dDG. The number of FosB positive cells in the dDG, decreased in infarcted mice, was significantly increased after chronic EE treatment. Chemogenetic activation of dDG neurons reduced anxiety and depressive-like behaviors in infarcted mice, while neuronal inhibition resulted in void of the anxiolytic and antidepressant effects of EE. Altogether, these findings indicated that dDG neurons may mediate EE-triggered anxiolytic and antidepressant effects in cortical infarcted mice.

The p75 neurotrophin receptor attenuates secondary thalamic damage after cortical infarction by promoting angiogenesis.

BACKGROUND: Angiogenesis is crucial in neuroprotection of secondary thalamic injury after cortical infarction. The p75 neurotrophin receptor (p75NTR) plays a key role in activating angiogenesis. However, the effects of p75NTR on angiogenesis in the thalamus after cortical infarction are largely unknown. Herein we investigate whether p75NTR facilitates angiogenesis to attenuate secondary thalamic damage via activating hypoxia-inducible factor 1α (HIF-1α)/vascular endothelial growth factor (VEGF) pathway mediated by Von Hippel-Lindau (VHL) after distal middle cerebral artery occlusion (dMCAO). METHODS: The male rat model of dMCAO was established. The effects of p75NTR on the angiogenesis was evaluated using RNA-sequencing, immunohistochemistry, western blot, quantitative real-time polymerase chain reaction, magnetic resonance imaging, behavior tests, viral and pharmacological interventions. RESULTS: We found that the p75NTR and vessel density were decreased in ipsilateral thalamus after dMCAO. The p75NTR-VHL interaction was reduced, which promoted the ubiquitination degradation of HIF-1α and reduced VEGF expression after dMCAO. Notably, p75NTR overexpression restrained the ubiquitination degradation of HIF-1α by inhibiting VHL-HIF-1α interaction, further promoted angiogenesis, increased cerebral blood flow of ipsilateral thalamus and improved neurological function after dMCAO. CONCLUSION: For the first time, we highlighted that the enhancement of p75NTR-VHL interaction promoted angiogenesis in attenuating secondary thalamic damage after dMCAO.

Early permanent cerebrospinal fluid diversion in aneurysmal subarachnoid hemorrhage: does a lower rate of nosocomial meningitis outweigh the risk of delayed cerebral vasospasm related morbidity?

Objective: Early permanent cerebrospinal fluid (CSF) diversion for hydrocephalus during the first 2 weeks after aneurysmal subarachnoid hemorrhage (aSAH) shortens the duration of external ventricular drainage (EVD) and reduces EVD-associated infections (EVDAI). The objective of this study was to detect any association with symptomatic delayed cerebral vasospasm (DCVS), or delayed cerebral ischemia (DCI) by the time of hospital discharge. Methods: We used a single-center dataset of aSAH patients who had received a permanent CSF diversion. We compared an 'early group' in which the procedure was performed up to 14 days after the ictus, to a 'late group' in which it was performed from the 15th day onward. Results: Among 274 consecutive aSAH patients, 39 (14%) had a permanent CSF diversion procedure with a silver-coated EVD. While the blood clot burden was similarly distributed, patients with early permanent CSF diversion (20 out of 39; 51%) had higher levels of consciousness on admission. Early permanent CSF diversion was associated with less colonized catheter, a shorter duration of extracorporeal CSF diversion (OR 0.73, 95%CI 0.58-0.92 per EVD day), and a lower rate of EVDAI (OR 0.08, 95%CI 0.01-0.80). The occurrence of CSF diversion device obstruction, the rate of symptomatic DCVS or detected DCI on computed tomography and the likelihood of a poor outcome at discharge did not differ between the two groups. Discussion: Early permanent CSF diversion lowers the occurrence of catheter colonization and infectious complication without affecting DCVS-related morbidity in good-grade aSAH patients. These findings need confirmation in larger prospective multicenter cohorts. Abbreviations: aSAH: aneurysmal subarachnoid hemorrhage; BNI: Barrow Neurological Institute Scale; CSF: Cerebrospinal fluid; DCVS: Delayed Cerebral Vasospasm; DCI: Delayed Cortical Ischemia; EKNZ: Ethik-Kommission Nordwest Schweiz; EVD: External ventricular drain; EVDAI: External ventricular drain-associated infections; GCS: Glasgow Coma Scale; IRB: Institutional Review Board; IVH: Inraventricular hemorrhage; mRS: Modified Rankin Scale; SOS: Swiss Study of Subarachnoid Hemorrhage Registry; WFNS: World Federation Neurological-Surgeon Scale.

Blockade of Nogo-A/Nogo-66 receptor 1 (NgR1) Inhibits Autophagic Activation and Prevents Secondary Neuronal Damage in the Thalamus after Focal Cerebral Infarction in Hypertensive Rats.

Focal cerebral infarction leads to autophagic activation, which contributes to secondary neuronal damage in the ipsilateral thalamus. Although Nogo-A deactivation enhances neuronal plasticity, its role in autophagic activation in the thalamus after ischemic stroke remains unclear. This study aimed to investigate the potential roles of Nogo-A/Nogo-66 receptor 1 (NgR1) in autophagic activation in the ipsilateral thalamus after cerebral infarction. Focal neocortical infarction was established using the middle cerebral artery occlusion (MCAO) method. Secondary damage in the ipsilateral thalamus was assessed by Nissl staining and immunostaining. The expression of Nogo-A, NgR1, Rho-A and Rho-associated coiled-coil containing protein kinase 1 (ROCK1) as well as autophagic flux were evaluated by immunofluorescence and immunoblotting. The roles of Nogo-A-NgR1 signaling in autophagic activation were determined by intraventricular delivery of an NgR1 antagonist peptide, NEP1-40, at 24 h after MCAO. The results showed that Nogo-A and NgR1 overexpression temporally coincided with marked increases in the levels of Beclin1, LC3-II and sequestosome 1 (SQSTM1)/p62 in the ipsilateral thalamus at seven and fourteen days after MCAO. In contrast, NEP1-40 treatment significantly reduced the expression of Rho-A and ROCK1 which was accompanied by marked reductions of LC3-II conversion as well as the levels of Beclin1 and SQSTM1/p62. Furthermore, NEP1-40 treatment significantly reduced neuronal loss and gliosis in the ipsilateral thalamus, and accelerated somatosensory recovery at the observed time-points after MCAO. These results suggest that blockade of Nogo-A-NgR1 signaling inhibits autophagic activation, attenuates secondary neuronal damage in the ipsilateral thalamus, and promotes functional recovery after focal cerebral cortical infarction.

Altered circular RNA expression profiles in the non-ischemic thalamus in focal cortical infarction mice.

Focal cerebral infarction leads to secondary changes in non-ischemic areas remote from but connected to the infarct site. Circular RNAs (circRNAs) are involved in the pathophysiological processes of many diseases. However, the expression and roles of circRNAs in non-ischemic remote regions after ischemic stroke remain unknown. In this study, adult male C57BL/6J mice were subjected to permanent distal middle cerebral artery occlusion (MCAO) to establish focal cortical infarction. High-throughput sequencing was used to profile the circRNA expression in the mouse ipsilateral thalamus at 7 and 14 d after MCAO. Bioinformatics analyses were conducted to predict the function of the differential expressed circRNAs' host and target genes. Compared with sham group, a total of 2659 circRNAs were significantly altered in the ipsilateral thalamus at 7 or 14 d after MCAO in mice. Among them, 73 circRNAs were significantly altered at both two time points after stroke. GO and KEGG analyses indicated that circRNAs plays important roles in secondary thalamic neurodegeneration and remodeling after focal cortical infarction. This is the first study to profile the circRNA expression in non-ischemic region of ischemic stroke, suggesting that circRNAs may be therapeutic targets for reducing post-stroke secondary remote neurodegeneration.

Ischemic stroke of the "hand knob area": A case series and literature review.

Isolated hand paresis may reflect an infarction of the "hand knob area", which represents less than 1% of all ischemic strokes. In this type of stroke, a potential source of embolism is often identified. There are no large case series regarding this topic in Latin America. Herein we present the largest cohort of this entity in the region and we compare our results with those previously published. We analyzed all stroke patients admitted to our hospital between May 2015 - June 2018. Only patients with motor +/- sensory deficits restricted to the hand and ischemic stroke confirmed by MRI were included. We assessed stroke mechanism, clinical characteristics and outcome. From 339 patients admitted with ischemic stroke, 12 (3.53%) were included (9 men, 75%). Mean age: 60.4 years-old (range:24-79). Localization of stroke: 8 patients (66%) precentral gyrus, 3 (25%) postcentral; in 1 both gyri were affected. Stroke mechanism according to TOAST classification was as follows: two patients (16%) large artery atherosclerosis, two cardioembolic, one other determined etiology (thrombophilia), seven (58%) undetermined etiology (SUE). Nine patients (75%) received antiplatelets and statins, and three (25%) anticoagulants. The mean follow-up period was 11 months (range 1-26). Stroke recurrence was observed in one patient. At follow up, eight patients (66%) had a modified Rankin Score (mRS) of 0 and one a mRS of 1. In conclusion, in this series the most prevalent stroke mechanism was SUE, mainly embolic stroke of undetermined source. The outcome was excellent regardless of stroke mechanism.

Clinicoradiological Correlation of Infarct Patterns on Diffusion-weighted Magnetic Resonance Imaging in Stroke.

Diffusion-weighted magnetic resonance imaging (DW-MRI) represents a major advance in the early diagnosis of acute ischemic stroke. It can detect edema due to ischemia in the brain tissue. It not only establishes the presence and location of ischemic brain injury but also a relatively new concept is the determination of infarct patterns seen on diffusion imaging and its clinical correlation. Objective To determine the frequency of various infarct patterns and their relationship with functional outcome of the patient. Materials and methods A total of 108 patients with acute stroke were enrolled by purposive sampling. Magnetic resonance imaging (MRI) was obtained with departmental protocol and diffusion-weighted sequences. The clinical data was collected from medical records and functional outcome was assessed at the time of admission using Barthel Index (BI) which was dichotomized into poor and favorable outcomes. The radiological data was collected and three infarct patterns (cortical, subcortical, and territorial infarcts) were recorded from diffusion-weighted images. Association of other risk factors such as age, gender, diabetes, hypertension (HTN), hyperlipidemia, and smoking were also evaluated. Results Amongst the three infarct patterns, subcortical infarcts were noted with the highest proportion of 62% (67/108). The highest proportion of territorial infarcts (78.6%) was significantly associated with a poor outcome in comparison to cortical and subcortical infarcts. Cortical infarcts (61.5%) were significantly associated with good outcomes followed by subcortical and then territorial infarcts (p-value < 0.002). Amongst the risk factors, HTN was found to be highly prevalent followed by diabetes mellitus (DM). Conclusion Subcortical infarct pattern was the most common, followed by territorial and cortical infarct. The highest proportion of infarct pattern with good outcomes was seen with cortical infarcts followed by subcortical and then territorial infarct pattern. HTN and coronary artery disease (CAD) were the effect modifiers showing significant association with poor outcomes.

Poststroke epilepsy following transient unilateral middle cerebral and common carotid artery occlusion in young adult and aged F344 rats.

The mechanisms of injured brain that establish poststroke seizures and epilepsy are not well understood, largely because animal modeling has had limited development. The main objective of this study was to determine whether an arterial occlusion model of cortical stroke in young adult and aged rats was capable of generating either focal or generalized epileptic seizures within 2 months of lesioning. Four- and 20-month-old male Fischer 344 (F344) sham-operated controls and those lesioned by transient (3 h) unilateral middle cerebral artery (MCA) and common carotid artery (CCA) occlusion (MCA/CCAo) were studied by video-EEG recordings up to 2 months post-procedure. The main findings were: 1) seizures (grade 3 and above) were recorded within 2 months in both young (4-month; 0.23/h) and aged (20-month; 1.93/h) MCA/CCAo rat groups; both MCA/CCAo rat groups had more seizures recorded than the respective control groups, i.e., no seizures in young controls and 0.52/h in old controls; 2) both age and infarction independently had effects on seizure frequency; however, there was no demonstrated interaction between the two factors; and 3) there was no difference in infarct volumes comparing 4- to 20-month-old MCA/CCAo animals. In addition, all lesioned and sham-operated animals demonstrated intermittent solitary myoclonic convulsions arising out of sleep. Morbidity and mortality of animals limited the extent to which the animals could be evaluated, especially 20-month-old animals. These results suggest that transient unilateral MCA/CCAo can result in poststroke epileptic seizures in both young adult and aged F344 rats within a relatively brief period of time following lesioning.

Transient and permanent arterial occlusions modeling poststroke epilepsy in aging rats.

The pathophysiological mechanisms of epileptogenesis following ischemic stroke in the aged brain are not well understood, largely due to limited developments in animal modeling of poststroke epilepsy (PSE). A recent study in our laboratory (Kelly et al., 2018) using transient (3 h) unilateral middle cerebral artery (MCA) and common carotid artery (CCA) occlusion (MCA/CCAo) in 4- and 20-month-old Fischer (F344) rats resulted in epileptic seizures in both age groups; age and infarction factors independently had effects on seizure frequency. We hypothesized that permanent unilateral MCA/CCAo, a simpler model, was capable of producing results comparable to those of transient MCA/CCAo. In this study, we performed permanent MCA/CCAo and compared it to transient MCA/CCAo in 76 4-, 12-, and 20-month-old F344 rats; 41 (54%) animals experienced early, unexpected mortality. The remaining 35 (46%) animals had depth electrodes implanted. Prior to implantation of depth electrodes, 9 (26%) of these 35 animals (26%) were monitored periodically by video alone before video-EEG monitoring (17,837 h total) to assess the potential development of PSE. No EEG recordings were obtained from 12- or 20-month-old transient occlusion or 20-month-old permanent occlusion animals due to premature deaths. Five animals (14%) demonstrated epileptic seizure activity after MCA/CCAo: one 4-month-old transient occlusion animal, one 4-month-old permanent occlusion animal, and three 12-month-old permanent occlusion animals. Of these 5 animals, all but the 4-month-old permanent animal demonstrated 1-4 Hz spike-wave discharges variably associated with inactivity or frank motor arrest, and 2 animals (4- and 12-month-old permanent) demonstrated generalized ictal EEG discharges associated with grade 5 convulsive activity. All animals monitored with video-EEG demonstrated generalized 7-9 Hz spike-wave discharges, innate in F344 animals and distinct from lesion-induced epileptic seizures. Gross inspection of brains revealed variability in lesion presence and size among age groups and occlusion types. Comparison of infarct volumes of permanent MCA/CCAo animals (2.9 ± 1.29 mm3, n = 6) with those of transient MCA/CCAo animals (1.7 ± 0.31 mm3, n = 3) was not significant (p = 0.44) due to the small sample size. Timm staining revealed no evidence of mossy fiber sprouting in 7 animals tested, only one of which was known to be epileptic (4-month-old transient). These results provide evidence of focal nonconvulsive electrographic ictal discharges and behavioral seizures in both permanent and transient MCA/CCAo animals lesioned at 4- or 12-months-of-age and support the use of arterial ligation as a viable method for modeling PSE.

Association of Perforator Infarction with Clinical Courses and Outcomes Following Surgical Clipping of Ruptured Anterior Communicating Artery Aneurysms.

BACKGROUND: Perforator infarction is a procedure-related complication of surgical clipping of ruptured anterior communicating artery (ACoA) aneurysms. Patients with perforator infarction may present with specific clinical features. The aim of this study was to elucidate incidence, risk factors, clinical course, and outcomes of perforator infarction following surgical clipping of ruptured ACoA aneurysms. METHODS: Retrospective analysis was performed of 104 patients from a single-center, observational cohort database who underwent surgical clipping for ruptured ACoA aneurysm. Risk factors of perforator infarction were identified. Correlation of perforator infarction with clinical course during hospitalization was investigated, focusing on dysfunction of hypothalamus and cerebral limbic system. We also evaluated any associations between perforator infarction and poor outcomes. RESULTS: Perforator infarction was observed in 24 (23.1%) patients. Use of temporary clip (P = 0.019, χ2 test) and intraoperative rupture (P < 0.001, χ2 test) were significantly associated with perforator infarction. Patients with perforator infarction had increased likelihood of hyponatremia (odds ratio 6.41 [95% confidence interval 2.27-18.1], P < 0.001) and insufficient oral intake (odds ratio 6.53 [95% confidence interval 1.80-23.7], P = 0.004) in the subacute stage of subarachnoid hemorrhage by multivariate analyses. Perforator infarction was an independent risk factor of poor functional outcomes at 3 months (modified Rankin Scale score 3-6; odds ratio 5.29 [95% confidence interval 1.62-17.2], P = 0.006). CONCLUSIONS: Perforator infarction following surgical clipping of ruptured ACoA aneurysms caused region-specific complications, including hyponatremia and insufficient oral intake, and was associated with poor functional outcomes.

Frecuencia y determinantes de epilepsia luego de un primer ictus isquémico arterial en una cohorte de niños / Frequency and risk factors for the development of epilepsy after an arterial ischemic stroke in a children's cohort

Existen pocos estudios evaluando los factores de riesgo para el desarrollo de epilepsia posterior a un ictus isquémico arterial (IIA) en la infancia. Objetivo: Evaluar los predictores clínicos y radiológicos para epilepsia post-ictus (EPI) en una cohorte de niños chilenos con un primer IIA. Metodología: Estudio analítico longitudinal observacional prospectivo de una cohorte de niños con diagnóstico de IIA entre 1 mes y 18 años, enrolados de forma consecutiva en la base de datos de Patología Cerebrovascular del Hospital Clínico de la Pontificia Universidad Católica de Chile entre los años 2003 y 2013. Todos los participantes con imágenes por resonancia magnética encefálica al momento del diagnóstico. Las variables estudiadas incluyeron características clínicas y radiológicas del evento agudo asociadas a EPI según estudios previos. Creamos un modelo multivariado por regresión logística para estimar los Odds Ratios (ORs) y sus respectivos intervalos de confianza al 95% (ICs) de cada variable estudiada para EPI (significancia <0,05). Resultados: De 81 niños reclutados, 41 (50,6%) con EPI. El análisis multivariado determinó que los predictores independientes de EPI incluyen edad menor al momento del IIA (OR=0,81; IC=0,69-0,95), ocurrencia de crisis sintomáticas agudas (OR=8,63; IC=2,03-36,7), infarto cortical (OR=17,2; IC=3,12-95,3) y arteriopatías del sistema nervioso central (OR=12; IC=1,47-97,8). Conclusiones: las crisis agudas, menor edad, infarto cortical y arteriopatías son factores de riesgo independientes para EPI en niños con un primer IIA.

Abstract. There are few studies evaluating the risk factors for the development of epilepsy after an arterial ischemic stroke (IIA) in childhood. Objective: To assess the clinical and radiological predictors for epilepsy post-stroke (EPI) in a cohort of Chilean children with a first IIA. Methodology: prospective observational longitudinal analytical study of a cohort of children with a IIA diagnosis, from 1 month to 18 years old, consecutively enrolled in the brain stroke database of the Hospital of the Pontificia Universidad Católica de Chile between 2003 and 2013. All participants had a brain magnetic resonance performed at the time of the diagnosis. The variables studied included clinical and radiological features of the acute event associated to EPI according to previous studies. We created a multivariate logistic regression model to estimate the Odds Ratios (ORs) and their respective intervals of confidence 95% (ICs) of each variable studied for EPI (significance < 0,05). Results: of 81 children recruited, 41 (50.6%) had EPI. The multivariate analysis determined that the independent predictors of PPE include: younger age at the time of the IIA (OR = 0. 81; IC = 0, 69-0, 95), occurrence of acute symptomatic crisis (OR = 8, 63; IC = 2, 03-36, 7), cortical infarction (OR = 17, 2; IC = 3, 12-95, 3) and arteriopathies of the central nervous system (OR = 12; IC = 1, 47-97, 8). Conclusions: acute crises, younger age, cortical infarction and arterial disease are independent risk factors for EPI in children with a first IIA.

Isolated Focal Cortical Infarction in a Patient with Churg-Strauss Syndrome

No abstract available.

Cortical infarction of the right parietal lobe and neurogenic heart disease: A report of three cases.

Three male patients were diagnosed with new cortical infarctions of the right parietal lobe on the basis of head magnetic resonance imaging; high-intensity signals indicating lesions in the right parietal lobe were noted on diffusion-weighted images at admission. Two of them presented with left hand weakness, and one exhibited left upper limb weakness. Treatment for improving blood supply to the brain was administered. One patient died suddenly because of ventricular fibrillation 3 days after admission. The other two patients had increased troponin levels and abnormal electrocardiograms, and were diagnosed with acute myocardial infarction half a month after admission. When lesions exist in field 7 of the parietal cortex (resulting in paralysis of the contralateral hand), the sympathetic center of the posterior lateral nucleus of the hypothalamus demonstrates compensatory excitement, which easily causes tachyarrhythmia and sudden death. Our experimental findings indicate that close electrocardiograph monitoring and cerebral infarction treatment should be standard procedures to predict and help prevent heart disease in patients with cerebral infarction in the right parietal lobe and left upper limb weakness as the main complaint.

Impairments of Inhibitory Motor Control in Cerebral Cortical Infarction

No abstract available.