Glycated serum protein is independently associated with progressive infarction in patients with acute ischemic stroke.

OBJECTIVE: This study investigated the relationship between glycated serum protein (GSP) and progressive infarction (PI). METHODS: From April 2017 to December 2020, we recruited 477 patients within 48 hours after the onset of acute ischemic stroke into this case-control study. Demographic characteristics, clinical information, and laboratory and neuroimaging data were recorded after admission. RESULTS: PI occurred in 144 (30.8%) patients. Patients with PI had higher initial National Institute of Health Stroke Scale (NIHSS) scores, higher discharge NIHSS scores, higher modified Rankin scale scores at 3 months after onset, higher GSP levels, lower prothrombin times, and lower creatinine levels than patients without PI. The likelihood of PI increased with increases in the GSP quartile. Multiple regression analysis revealed that high GSP levels (>2.14 mmol/L) were independently associated with PI. Subgroup analyses identified high GSP levels as an independent predictor of PI in patients with large artery atherosclerosis (third quartile: odds ratio [OR] = 3.793; 95% confidence interval [CI] = 1.555-9.250; fourth quartile: OR = 2.675; 95% CI = 1.056-6.776) and anterior circulation small vessel occlusion (fourth quartile: OR = 13.859; 95% CI = 2.024-94.885). CONCLUSIONS: GSP might be an independent predictor for PI in certain patients with acute ischemic stroke.

Estimation of prognosis in patients after decompressive craniectomy after malignant hemispheric infarction: multifactorial scoring scale.

BACKGROUND: Patient's age is considered to be one of the most relevant factors in selecting surgical candidates for decompressive hemicraniectomy after malignant hemispheric infarction. However, questions about surgical indication in older patients, patients with consciousness disorder or patients with large infarctions remain unanswered. OBJECTIVE: Our aim was to design a multifactorial scoring scale based on a combination of patient-specific factors in order to optimize the assessment of prognosis in patients after hemicraniectomy malignant strokes. METHODS: In this prospective observational study with a one-year follow-up, we assessed clinical and imaging data of patients who underwent decompressive hemicraniectomy due to malignant brain infarction. Barthel index was used as a single outcome measure to distinguish favorable vs. unfavorable outcomes. Associations between multiple variables and clinical outcome were assessed. Subsequently, a design of a predictive scoring system was proposed. RESULTS: Age of the patient, preoperative level of consciousness, midline shift, and volume of infarction showed a significant association with postoperative Barthel index. According to the identified factors, a multifactorial prognostic scoring system was introduced, aimed to distinguish between favorable and unfavorable outcomes. Using ROC analysis, it has achieved an AUC of 0.74 (95%CI 0.58‒0.89, p=0.01)CONCLUSIONS: Prediction of postoperative outcome should be based on multiple variables. Our scale, based on the clinical and imaging data, can be used during decision-making to estimate potential benefit of decompressive craniectomy in patients after malignant brain infarction (Tab. 5, Fig. 1, Ref. 32). Text in PDF www.elis.sk Keywords: decompressive hemicraniectomy, malignant hemispheric infarction, indication, outcome, prediction.

Transverse spinal cord infarction following immunoglobulin treatment in a patient with exfoliative dermatitis: A case report.

RATIONALE: Transverse spinal cord infarction (SCI) is rare but highly disabling. Aortic thrombosis was described as one of the most common etiologies. Thromboembolic complications associated with intravenous immunoglobulin (IVIG) have been reported. PATIENT CONCERNS: A previously well, 64-year-old man who was given the treatment of IVIG (0.4 g/kg/d for 5 days) for exfoliative dermatitis 2 weeks before, progressively developed flaccid paraplegia of lower extremities, loss of all sensations below T3 level and urinary incontinence within 50 minutes. DIAGNOSES: A diagnosis of SCI and pulmonary embolism was made. IVIG was considered the possible cause. INTERVENTIONS: Anticoagulation treatment and continuous rehabilitation were administered. OUTCOMES: The neurologic deficiency of the patient was partially improved at the 3-year follow-up. LESSONS: The rapid development of severe deficits within 4 hours mostly contributes to the diagnosis of SCI. Heightened awareness of possible thrombotic events is encouraged for a month-long period following IVIG therapy.

A 38-Year-Old Woman With REM Predominant Central Sleep Apnea After Bulbar Infarction.

CASE PRESENTATION: A 38-year-old previously healthy woman was referred to our sleep center for recurrent witnessed breathing arrest during sleep. She had been brought to the ED 3 months earlier because of sudden onset of dizziness with nausea and vomiting, numbness and weakness of the left limb, less clear speech, double vision, dysphagia, and choking cough while drinking water. Brain MRI showed an acute cerebral infarction in the left medulla oblongata (Fig 1). High-resolution MRI showed vertebral artery dissection (Fig 2). Antiplatelet aggregation, lipid reduction, plaque stabilization, and trophic nerve treatments were administered, and the left limb strength, speech, and swallowing function improved. She complained of poor sleep and difficulties with memory.

Shen Shuai II recipe improves renal hypoxia to attenuate renal injury in 5/6 renal ablation/infarction rats and effect evaluation using blood oxygenation level-dependent functional magnetic resonance imaging.

Background: Renal hypoxia plays a key role in the progression of chronic kidney disease (CKD). Shen Shuai II Recipe (SSR) has shown good results in the treatment of CKD as a common herbal formula. This study aimed to explore the effect of SSR on renal hypoxia and injury in CKD rats. Methods: Twenty-five Wistar rats underwent 5/6 renal ablation/infarction (A/I) surgery were randomly divided into three groups: 5/6 (A/I), 5/6 (A/I) + losartan (LOS), and 5/6 (A/I) + SSR groups. Another eight normal rats were used as the Sham group. After 8-week corresponding interventions, blood oxygenation level-dependent functional magnetic resonance imaging (BOLD-fMRI) was performed to evaluate renal oxygenation in all rats, and biochemical indicators were used to measure kidney and liver function, hemoglobin, and proteinuria. The expression of fibrosis and hypoxia-related proteins was analyzed using immunoblotting examination. Results: Renal oxygenation, evaluated by BOLD-fMRI as cortical and medullary T2* values (COT2* and MET2*), was decreased in 5/6 (A/I) rats, but increased after SSR treatment. SSR also downregulated the expression of hypoxia-inducible factor-1α (HIF-1α) in 5/6 (A/I) kidneys. With the improvement of renal hypoxia, renal function and fibrosis were improved in 5/6 (A/I) rats, accompanied by reduced proteinuria. Furthermore, the COT2* and MET2* were significantly positively correlated with the levels of creatinine clearance rate (Ccr) and hemoglobin, but negatively associated with the levels of serum creatinine (SCr), blood urea nitrogen (BUN), serum cystatin C (CysC), serum uric acid (UA), 24-h urinary protein (24-h Upr), and urinary albumin:creatinine ratio (UACR). Conclusion: The degree of renal oxygenation reduction is correlated with the severity of renal injury in CKD. SSR can improve renal hypoxia to attenuate renal injury in 5/6 (A/I) rats of CKD.

Clinical study of tirofiban compared to low molecular weight heparin in the antithrombotic treatment of progressive pontine infarction.

OBJECTIVE: To investigate the efficacy and safety of tirofiban and low molecular weight heparin (LMWH) in the treatment of patients undergoing acute progressive pontine infarction. PATIENTS AND METHODS: Patients with acute progressive pontine infarction who were hospitalized in the Neurology Department from June 2021 to June 2023 were included in the study and randomly divided into two groups, namely the experimental group (tirofiban group) and the control group (LMWH group). All patients in both groups were required to receive conventional comprehensive treatment and dual antiplatelet therapy with aspirin + clopidogrel at the beginning of admission. The National Institutes of Health Stroke Scale (NIHSS) score and Barthel Index (BI) were used to evaluate the neurological deficits on the first day of admission, the next day with stroke progression, and at discharge after treatment with tirofiban and LMWH, respectively in the two groups. The modified Rankin Scale was employed to assess prognosis on the 90th day after treatment. Clinical adverse events were followed up for 90 days, comparing the clinical efficacy and safety of the two treatment methods. RESULTS: There was no statistical significance in NIHSS score and Barthel Index between the tirofiban group and the LMWH group on the first day of admission and the next day with stroke progression (p > 0.05). After stroke progression, tirofiban and LMWH were separately used for treatment in the two groups. We found that the NIHSS score of the tirofiban group was lower than that of the LMWH group, and the Barthel Index score was higher than that of the LMWH group at discharge (p < 0.05). After three months of follow-up, the mRS score of the tirofiban group was dramatically higher than that of the LMWH group (p < 0.05). No significant harmful or adverse reactions, such as bleeding events, were found in the two groups (p > 0.05). CONCLUSIONS: Tirofiban may be more effective and safer than LMWH in controlling the progression of acute pontine infarction, but further and large-sample studies are still needed to confirm this finding.

Metabolic Imaging of Acute Ischemic Stroke (PET, 1Hydrogen Spectroscopy, 17Oxygen Imaging, 23Sodium MRI, pH Imaging).

Acute stroke imaging plays a vital and time-sensitive role in therapeutic decision-making. Current clinical workflows widely use computed tomography (CT) and magnetic resonance (MR) techniques including CT and MR perfusion to estimate the volume of ischemic penumbra at risk for infarction without acute intervention. The use of imaging techniques aimed toward evaluating the metabolic derangements underlying a developing infarct may provide additional information for differentiating the penumbra from benign oligemia and infarct core. The authors review several modalities of metabolic imaging including PET, hydrogen and oxygen spectroscopy, sodium MRI, and pH-weighted MRI.

Thrombolysis increases the risk of persistent headache attributed to ischemic stroke: A prospective observational study.

BACKGROUND AND OBJECTIVE: Persistent headache attributed to ischemic stroke (PHPIS) is increasingly acknowledged and was added to the 2018 ICHD-3. Intravenous thrombolysis (IVT) is a common treatment for acute ischemic stroke. It remains unknown whether this treatment influences the occurrence of a persistent poststroke headache. We aimed to describe the incidence and clinical characteristics of persistent headaches occurring after acute ischemic stroke in patients with or without IVT and explore the risk factors. METHODS: A prospective observational study was performed between the 234 individuals who received IVT and 226 individuals without IVT in 5 stroke units from Wuhan, China. Subjects were followed for 6 months after stroke via a structured questionnaire. RESULTS: Age, gender, vascular risk factors, and infarct location/ circulation distribution did not differ between the groups, although IVT group had higher initial NIHSS scores. At the end of the follow-up, 12.0% (55/460) of subjects reported persistent headaches after ischemic stroke. The prevalence of persistent headache was significantly higher in the IVT group than non-IVT group (15.4% vs. 8.4%, p = .021). Patients with younger age (p = .033; OR 0.97; 95% CI 0.939-0.997), female sex (p = .007; OR 2.40; 95% CI 1.269-4.520), posterior circulation infarct (p = .024; OR 2.19; 95% CI 1.110-4.311), and IVT (p = .005; OR 2.51; 95% CI 1.313-4.782) were more likely to develop persistent headache after ischemic stroke. CONCLUSION: The potential influence of IVT should be considered when assessing persistent poststroke headache. Future studies will investigate the underlying mechanisms.

Effect of Peri-operative Blood Transfusion on Neurological Outcome Following Aneurysmal Subarachnoid Hemorrhage: A Prospective Observational Study.

BACKGROUND: Anemia is a common complication of aneurysmal subarachnoid hemorrhage and is associated with unfavorable outcomes. Whether the physiological benefits of transfusion for anemia surpass the risk of blood transfusion remains to be determined. OBJECTIVES: The primary outcome was to evaluate the impact of peri-operative blood transfusion on the long-term neurological outcome, assessed by Glasgow Outcome Scale Extended at 3 months. The secondary outcomes included the impact of transfusion on the short-term neurological outcome, assessed by Modified Rankin Score at discharge/7 days, and on the incidence of vasospasm, infarction, re-exploration, tracheostomy, and length of hospital stay. MATERIAL AND METHODS: This prospective observational study was conducted on 185 patients with aneurysmal subarachnoid hemorrhage undergoing clipping of the aneurysmal neck. In our study, blood transfusion was administered to keep the target Hb around 10 g/dL. RESULTS: Unfavorable long-term outcome was found in 27/97 (28%) of patients who received a blood transfusion as compared to 13/74 (18%) of patients who did not receive a transfusion (P = 0.116). Patients receiving transfusion had more chances of an unfavorable outcome at discharge/7 days as compared to those not transfused [44/103 (43%) versus 22/80 (27%)], P = 0.025. There were increased chances of vasospasm, infarction, re-exploration, tracheostomy, and increased length of hospital stay in patients receiving transfusion (P < 0.05). CONCLUSIONS: The use of blood transfusion in patients with aneurysmal subarachnoid hemorrhage was associated with increased neurological complications and hence an unfavorable short-term outcome. However, when used judiciously as per the clinical requirements, blood transfusion did not have a significant effect on long-term neurological outcome.

Superficial small cerebellar infarcts in cerebral amyloid angiopathy on 3 T MRI: A preliminary study.

BACKGROUND: Strictly superficial cerebellar microbleeds and cerebellar superficial siderosis have been considered markers of advanced cerebral amyloid angiopathy (CAA), but there are few studies on cerebellar ischemic lesions in CAA. We investigated the presence of superficial small cerebellar infarct (SCI) ≤15 mm and its relation to magnetic resonance imaging (MRI) markers in patients with probable CAA. METHODS: Eighty patients with probable CAA were retrospectively evaluated. The presence of superficial SCIs was examined, along with cerebellar microbleeds and cerebellar superficial siderosis, using 3-T MRI. Lobar cerebral microbleeds, cortical superficial siderosis (cSS), enlargement of the perivascular space in the centrum semiovale, and white matter hyperintensity were assessed and the total CAA-small vessel disease (SVD) score was calculated. RESULTS: Nine of the 80 patients (11.3%) had a total of 16 superficial SCIs. By tentatively defining SCI <4 mm as cerebellar microinfarcts, 8 out of 16 (50%) superficial SCIs corresponded to cerebellar microinfarcts. The total CAA-SVD score was significantly higher in patients with superficial SCIs (p = 0.01). The prevalence of cSS (p = 0.018), cortical cerebral microinfarct (p = 0.034), and superficial cerebellar microbleeds (p = 0.006) was significantly higher in patients with superficial SCIs. The number of superficial cerebellar microbleeds was also significantly higher in patients with superficial SCIs (p = 0.001). CONCLUSIONS: Our results suggest that in patients with CAA, superficial SCIs (including microinfarcts) on MRI may indicate more severe, advanced-stage CAA. These preliminary findings should be verified by larger prospective studies in the future.

Deviation From Personalized Blood Pressure Targets Correlates With Worse Outcome After Successful Recanalization.

BACKGROUND: Personalized blood pressure (BP) management for patients with acute ischemic stroke after successful endovascular thrombectomy lacks evidence. We aimed to investigate whether the deviation of BP from cerebral autoregulation limits is associated with worse outcomes. METHODS AND RESULTS: We determined autoregulation by measuring mean velocity index and calculated the percentage of time and the burden (defined as the time-BP area) with BP outside the autoregulatory limits of each subject within 48 hours after endovascular thrombectomy. In total, 91 patients with large vessel occlusion stroke who had achieved successful recanalization were prospectively enrolled between May 2020 and February 2022. The burden with BP outside the autoregulatory limits was associated with poor outcome (modified Rankin Scale score 3-6) at 90 days (adjusted odds ratio, 1.28 [95% CI, 1.03-1.59]). The percentage of time with BP out of the autoregulatory limits was correlated with early neurological deterioration (National Institute of Health Stroke Scale scores increased ≥2 at 7 days) (adjusted odds ratio, 1.38 [95% CI, 1.04-1.83]). The burden of BP that decreased below the autoregulatory lower limit was associated with significant infarct growth (volume of infarct growth >11.6 mL) at 7 days (adjusted odds ratio, 1.21 [95% CI, 1.01-1.44]). The percentage of time that BP exceeded the autoregulatory upper limit was associated with symptomatic intracranial hemorrhage within 48 hours (adjusted odds ratio, 1.55 [95% CI, 1.02-2.34]). CONCLUSIONS: Both the percentage of time and the burden of BP that deviates from the autoregulation-preserved range are associated with unfavorable clinical outcomes. This study highlights the potential benefits of autoregulation-guided BP management strategy after successful recanalization.

[Medullary infarction secondary to endovascular treatment of thoracoabdominal aortic aneurysm] / Infarto medular secundario a tratamiento endovascular de aneurisma de aorta toraco-abdominal.

Medullary infarction is a severe and infrequent pathology, which represents 1% of all ischemic strokes, and is also a rare complication of different surgical procedures. It is caused by the acute interruption of the blood flow of the spinal cord, manifesting itself with clinical neurological deficits related to the affected vascular territory. Methods: We present the case of an 80-year-old patient, with cardiovascular risk factors, who is present on post-surgical day 13, after placement of a vascular endoprosthesis for a thoracoabdominal aneurysm, sudden appearance of paraparesis with progression to paraplegia and hypoesthesia in both lower extremities. CT angiography of the aorta rules out local complications in the endoprosthesis. Medullary MRI showed images compatible with acute dorsal medullary infarction from level D9. Results: On discharge, the patient presented paraplegia and hypoesthesia of both lower extremities with fecal and urinary incontinence. Conclusion: Spinal cord infarction may be limited to a vascular territory or be more extensive according to its pathogenesis. The affectation of the anterior spinal artery is the most common and is characterized by bilateral motor deficits and loss of thermoalgesic sensitivity, which could have a great impact on the quality of life of patients. Its etiology is varied, including aortic surgery within its causes. MRI is very useful for its diagnosis and currently there are no clinical guides for the optimal treatment.

Introducción: El infarto medular es una patología severa e infrecuente, que representa el 1% del total de ictus isquémicos, siendo además una complicación rara de distintos procedimientos quirúrgicos. Es causado por la interrupción aguda del flujo sanguíneo de la médula espinal, manifestándose con déficits neurológicos clínicos relacionados con el territorio vascular afectado. Métodos: Presentamos el caso de un paciente de 80 años, con factores de riesgo cardiovascular, quien presenta en día postquirúrgico 13, tras colocación de endoprótesis vascular por aneurisma toraco-abdominal aparición brusca de paraparesia con progresión a paraplejía e hipoestesia en ambas extremidades inferiores.  Angio-TC de aorta descarta complicación local en la endoprótesis. RM medular mostró imágenes compatibles con Infarto agudo de médula dorsal desde el nivel D9. El paciente no fue subsidiario de tratamiento revascularizador. El tratamiento consistió en medidas de soporte. Resultados: Al alta el paciente presentaba paraplejia e hipoestesia de ambas extremidades inferiores con incontinencia fecal y urinaria. Conclusión: El infarto de la médula espinal puede estar limitado a un territorio vascular o estar más extendido según su patogenia. La afectación de la arteria espinal anterior es la más común y se caracteriza por déficits motores bilaterales y pérdida de la sensibilidad termoalgésica, pudiendo llegar a producir un gran impacto en la calidad de vida de los pacientes. Su etiología es variada, incluyéndose la cirugía aórtica dentro de sus causas. La RM es muy útil para su diagnóstico y actualmente no existen guías clínicas para el tratamiento óptimo.

LOX-1 and MMP-9 Inhibition Attenuates the Detrimental Effects of Delayed rt-PA Therapy and Improves Outcomes After Acute Ischemic Stroke.

BACKGROUND: Acute ischemic stroke triggers endothelial activation that disrupts vascular integrity and increases hemorrhagic transformation leading to worsened stroke outcomes. rt-PA (recombinant tissue-type plasminogen activator) is an effective treatment; however, its use is limited due to a restricted time window and hemorrhagic transformation risk, which in part may involve activation of MMPs (matrix metalloproteinases) mediated through LOX-1 (lectin-like oxLDL [oxidized low-density lipoprotein] receptor 1). This study's overall aim was to evaluate the therapeutic potential of novel MMP-9 (matrix metalloproteinase 9) ± LOX-1 inhibitors in combination with rt-PA to improve stroke outcomes. METHODS: A rat thromboembolic stroke model was utilized to investigate the impact of rt-PA delivered 4 hours poststroke onset as well as selective MMP-9 (JNJ0966) ±LOX-1 (BI-0115) inhibitors given before rt-PA administration. Infarct size, perfusion, and hemorrhagic transformation were evaluated by 9.4-T magnetic resonance imaging, vascular and parenchymal MMP-9 activity via zymography, and neurological function was assessed using sensorimotor function testing. Human brain microvascular endothelial cells were exposed to hypoxia plus glucose deprivation/reperfusion (hypoxia plus glucose deprivation 3 hours/R 24 hours) and treated with ±tPA and ±MMP-9 ±LOX-1 inhibitors. Barrier function was assessed via transendothelial electrical resistance, MMP-9 activity was determined with zymography, and LOX-1 and barrier gene expression/levels were measured using qRT-PCR (quantitative reverse transcription PCR) and Western blot. RESULTS: Stroke and subsequent rt-PA treatment increased edema, hemorrhage, MMP-9 activity, LOX-1 expression, and worsened neurological outcomes. LOX-1 inhibition improved neurological function, reduced edema, and improved endothelial barrier integrity. Elevated MMP-9 activity correlated with increased edema, infarct volume, and decreased neurological function. MMP-9 inhibition reduced MMP-9 activity and LOX-1 expression. In human brain microvascular endothelial cells, LOX-1/MMP-9 inhibition differentially attenuated MMP-9 levels, inflammation, and activation following hypoxia plus glucose deprivation/R. CONCLUSIONS: Our findings indicate that LOX-1 inhibition and ± MMP-9 inhibition attenuate negative aspects of ischemic stroke with rt-PA therapy, thus resulting in improved neurological function. While no synergistic effect was observed with simultaneous LOX-1 and MMP-9 inhibition, a distinct interaction is evident.

The lncRNA lnc_AABR07044470.1 promotes the mitochondrial-damaged inflammatory response to neuronal injury via miR-214-3p/PERM1 axis in acute ischemic stroke.

PURPOSE: We investigated the role of lnc_AABR07044470.1 on the occurrence and development of acute ischemic stroke (AIS) and neuronal injury by targeting the miR-214-3p/PERM1 axis to find a novel clinical drug target and prediction and treatment of AIS. METHODS: The mouse AIS animal model was used in vivo experiments and hypoxia/reoxygenation cell model in vitro was established. Firstly, infarction volume and pathological changes of mouse hippocampal neurons were detected using HE staining. Secondly, rat primary neuron apoptosis was detected by flow cytometry assay. The numbers of neuron, microglia and astrocytes were detected using immunofluorescence (IF). Furthermore, binding detection was performed by bioinformatics database and double luciferase reporter assay. Lnc_AABR07044470.1 localization was performed using fluorescence in situ hybridization (FISH).Lnc_AABR07044470.1, miR-214-3pand PERM1mRNA expression was performed using RT-qPCR. NLRP3, ASC, Caspase-1 and PERM1 protein expression was performed using Western blotting. IL-1ß was detected by ELISA assay. RESULTS: Mouse four-vessel occlusion could easily establish the animal model, and AIS animal model had an obvious time-dependence. HE staining showed that, compared with the sham group, infarction volume and pathological changes of mouse hippocampal neurons were deteriorated in the model group. Furthermore, compared with the sham group, neurons were significantly reduced, while microglia and astrocytes were significantly activated. Moreover, the bioinformatics prediction and detection of double luciferase reporter confirmed the binding site of lnc_AABR07044470.1 to miR-214-3p and miR-214-3p to Perm1. lnc_AABR07044470.1 and PERM1 expression was significantly down-regulated and miR-214-3pexpression was significantly up-regulated in AIS animal model in vivo. At the same time, the expression of inflammasome NLRP3, ASC, Caspase-1 and pro-inflammatory factor IL-1ß was significantly up-regulated in vivo and in vitro. The over-expression of lnc_AABR07044470.1 and miR-214-3p inhibitor could inhibit the neuron apoptosis and the expression of inflammasome NLRP3, ASC, Caspase-1 and pro-inflammatory factor IL-1ß and up-regulate the expression of PERM1 in vitro. Finally, over-expression of lnc_AABR07044470.1 and miR-214-3p inhibitor transfected cell model was significant in relieving the AIS and neuronal injury. CONCLUSION: Lnc_AABR07044470.1 promotes inflammatory response to neuronal injury via miR-214-3p/PERM1 axis in AIS.

A 78-Year-Old Woman with Sudden Onset of Left-Sided Hemiballismus.

BACKGROUND Hemiballismus is the most severe form of chorea and is a hyperkinetic disorder characterized by involuntary, high-amplitude movements of the ipsilateral arm and leg, due to lesions of the contralateral side of the central nervous system. Ischemic or hemorrhagic strokes and nonketotic hyperglycemia are predominant etiologies of hemiballismus. Case reports highlighting hemiballismus associated with temporal and parietal lobe infarcts have been published, although research of frontal lobe involvement is limited. CASE REPORT A 78-year-old woman presented to the Emergency Department with sudden-onset left-sided hemiballismus. On examination, she was alert, oriented to self and time, and able to follow commands. Her neurologic examination was notable for left-sided hemiballismus, described by the provider as periodic, uncontrolled, and involving a "flinging" motion of the left upper and lower extremities, sparing the face. She was treated with benzodiazepines in the Emergency Department and administered intravenous levetiracetam. Computed tomography of the head without contrast revealed an old left basal ganglia lacunar infarct. The patient was then admitted to the inpatient service, where magnetic resonance imaging of the brain revealed an acute punctate left superior frontal gyrus cortical infarct. Outpatient electroencephalogram revealed right anterior hemisphere dysfunction. CONCLUSIONS We describe a patient with left-sided sudden onset hemiballismus with an acute infarct of the ipsilateral superior frontal gyrus. This case highlights that brain lesions separate from the basal ganglia can induce hemiballismus, particularly within the frontal lobe, which warrants further research into precentral sulcus functioning and its role in modulating motor activity.

Brain frailty associated with stroke events in anterior circulation large artery occlusion.

OBJECTIVE: To investigate the factors associated with brain frailty and the effect of brain frailty in patients with anterior circulation large artery occlusion (AC-LAO). METHODS: 1100 patients with AC-LVO consecutively admitted to the Second Hospital of Hebei Medical University, North China between June 2016 and April 2018 were retrospectively analyzed. The variables associated with brain frailty and stroke outcome were analyzed by ANOVA analysis, the Mann-Whitney U test and multiple linear regression. Based on previous research. Brain frailty score comprises 1 point each for white matter hyperintensity (WMH), old infarction lesions, and cerebral atrophy among 983 participants with baseline brain magnetic resonance imaging or computed tomography. RESULTS: Among AC-LAO participants, baseline brain frailty score ≥ 1 was common (750/983, 76.3%). Duration of hypertension > 5 years (mean difference [MD] 0.236, 95% CI 0.077, 0.395, p = 0.004), multiple vessel occlusion (MD 0.339, 95% CI 0.068, 0.611, p = 0.014) and basal ganglia infarction (MD -0.308, 95% CI -0.456, -0.160, p < 0.001) were independently associated with brain frailty score. Brain frailty score was independently associated with stroke events, and higher brain frailty scores were associated with higher rates of stroke events (p < 0.001). However, brain frailty has no independent effect on short-term outcome of ACI in AC-LAO patients. CONCLUSIONS: In AC-LAO patients, older age, duration of hypertension > 5 years, and multiple vessel occlusion influenced the brain frailty score. Brain frailty score was independently associated with the occurrence of stroke events in AC-LAO patients.

[Colchicine alleviates myocardial ischemia-reperfusion injury in mice by activating AMPK].

OBJECTIVE: To investigate the protective effect of colchicine against myocardial ischemia-reperfusion injury (I/R) and explore the underlying mechanism. METHODS: H9C2 cells exposed to hypoxia/reoxygenation (H/R) were treated with 3 nmol/L colchicine, after which the changes in cell viability were assessed using MTT assay, and AMPK phosphorylation, the expressions of NOX4, NRF2, SOD2, BAX, Bcl-2, and cleaved caspase-3 were detected with Western blotting. Male C57BL/6 mice were randomized into sham operation, I/R, I/R+colchicine, and I/R+colchicine+dorsomorphin (DSMP) groups. After the treatments, myocardial expressions of p-AMPK/AMPK, 8-OHdG, cleaved caspase-3, mitochondrial BAX (Mito-BAX), and cytoplasmic cytochrome C (Cyt-Cyto C) were examined and cardiac functions, infarct area, ATP content, and serum levels of lactic dehydrogenase (LDH) and cardiac troponin T (cTnT) levels were assessed. RESULTS: In H9C2 cells, H/R exposure significantly reduced AMPK phosphorylation and expressions of NRF2, SOD2, and Bcl-2, lowered cell viability, and up-regulated the expressions of NOX4, BAX, and cleaved caspase-3 (P < 0.05), and these changes were obviously alleviated by colchicine treatment (P < 0.05). In the mouse models, myocardial I/R injury significantly reduced myocardial AMPK phosphorylation level, ATP content, and expressions of NRF2, SOD2 and Bcl-2, caused cardiac function impairment, enhanced NOX4, Mito-BAX, Cyt-Cyto C, BAX, 8-OHdG, and cleaved caspase-3 expressions, and increased infarct area and serum LDH and cTnT levels (P < 0.05). Colchicine treatment significantly reversed the damaging effects of I/R (P < 0.05), but its protective effects was obviously antagonized by DSMP (P < 0.05). CONCLUSION: Colchicine alleviates myocardial I/R injury and protects cardiac function in mice by reducing myocardial oxidative stress and apoptosis via activating AMPK.

Reduced cerebral blood flow and cognitive dysfunction following isolated cerebellar infarction: two case reports.

Cognitive impairment in focal cerebellar disorders has been widely recognized and is described as cerebellar cognitive affective syndrome (CCAS). However, the relationship between CCAS and crossed cerebello-cerebral diaschisis (CCD) has rarely been discussed. The present report describes the uncommon phenomenon of CCD in two cases with isolated cerebellar infarction, and discuss its contribution to cognitive impairment. Cognitive performance was examined using the CCAS scale and a battery of neuropsychological assessments. Moreover, the relative distribution of cerebral and cerebellar blood flow was measured using three-dimensional arterial spin labeling imaging. Case 1 showed deficits in general cognition and had impaired language, episodic memory, and executive function. Case 2 showed deficits in general cognition at baseline, and cognitive deterioration of visuospatial abilities, language, episodic memory, and executive function was observed at the 3-month follow-up. Both cases met the diagnosis criteria of CCAS. Reduced cerebral blood flow was observed in the cerebral hemisphere contralateral to the cerebellar infarction at baseline in Case 1, and at the 3-month follow-up in Case 2. The present report describes cognitive decline after isolated cerebellar infarction in combination with contralateral cerebral hypoperfusion, as measured using quantitative arterial spin labeling. One possible mechanism involves the functional depression of cerebello-cerebral pathways.