Journal articles: 'Long-Term cerebral effect'

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Ye, Fei, Guan-Shui Bao, Heng-Shi Xu, and Pan-Pan Deng. "Effect of platelet count on long-term prognosis of cerebral infarction." Restorative Neurology and Neuroscience 38, no. 3 (August 20, 2020): 265–70. http://dx.doi.org/10.3233/rnn-200993.

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Objective: This study aimed to analyze the correlation between platelet (PLT) count and the modified Rankin scale (mRS) in patients with cerebral infarction (CI) at the later stage of rehabilitation, which can be used to guide the secondary prevention strategy of CI. Methods: A total of 180 CI patients were divided into three groups according to PLT count: low PLT group (<125×109/L), medium PLT group (126– 225×109/L) and high PLT group (>226×109/L). The mRS was evaluated after three months and one year, respectively, and the difference in long-term prognosis between groups was analyzed. The mRS is an ordered scale coded from 0 (no symptoms at all) through 5 (severe disability) 6 (death). Results: Finally, a total of 99 patients had complete data. The results of the multiple comparisons among the three groups were as follows: the analysis of variance of the mRS at three months after onset yielded F = 6.714 and P = 0.002, and the difference was statistically significant. The mRS was lowest in the medium PLT group (2.09±1.465), and neurological function recovery was the best. After one year, the mRS for the medium PLT group was the lowest (1.49±1.523), with F = 6.860 and P = 0.002. The repeated measures analysis of variance revealed that the effect of continuous rehabilitation was significant in the interval from three months to one year after onset (F = 35.528, P < 0.001). This was very significant, especially for patients taking aspirin (F = 50.908, P < 0.001). However, for patients who did not take aspirin, the effect of continuous rehabilitation was not obvious during the nine months, and the difference between the results of two mRS measurements was not statistically significant (F = 1.089, P = 0.308). Conclusions: Patients with a PLT count of 126– 225×109/L had the lowest mRS between three months and one year after onset, but had the best recovery of nerve function. Patients who persisted in taking aspirin continued to significantly recover during the 9-month period, from three months to one year after onset. Aspirin is not only a secondary preventive drug, but also an important drug to promote the rehabilitation of CI patients.

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Espeland, Mark A., Jose A. Luchsinger, Rebecca H. Neiberg, Owen Carmichael, Paul J. Laurienti, Xavier Pi‐Sunyer, Rena R. Wing, et al. "Long Term Effect of Intensive Lifestyle Intervention on Cerebral Blood Flow." Journal of the American Geriatrics Society 66, no. 1 (October 30, 2017): 120–26. http://dx.doi.org/10.1111/jgs.15159.

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Yrjänheikki, Juha, Jari Koistinaho, Mikko Kettunen, Risto A. Kauppinen, Kurt Appel, Michael Hüll, and Bernd L. Fiebich. "Long-term protective effect of atorvastatin in permanent focal cerebral ischemia." Brain Research 1052, no. 2 (August 2005): 174–79. http://dx.doi.org/10.1016/j.brainres.2005.06.004.

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Ahnstedt, Hilda, Maryam Mostajeran, Frank W. Blixt, Karin Warfvinge, Saema Ansar, Diana N. Krause, and Lars Edvinsson. "U0126 Attenuates Cerebral Vasoconstriction and Improves Long-Term Neurologic Outcome after Stroke in Female Rats." Journal of Cerebral Blood Flow & Metabolism 35, no. 3 (March 2015): 454–60. http://dx.doi.org/10.1038/jcbfm.2014.217.

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Sex differences are well known in cerebral ischemia and may impact the effect of stroke treatments. In male rats, the MEK1/2 inhibitor U0126 reduces ischemia-induced endothelin type B (ETB) receptor upregulation, infarct size and improves acute neurologic function after experimental stroke. However, responses to this treatment in females and long-term effects on outcome are not known. Initial experiments used in vitro organ culture of cerebral arteries, confirming ERK1/2 activation and increased ETB receptor-mediated vasoconstriction in female cerebral arteries. Transient middle cerebral artery occlusion (tMCAO, 120 minutes) was induced in female Wistar rats, with U0126 (30 mg/kg intraperitoneally) or vehicle administered at 0 and 24 hours of reperfusion, or with no treatment. Infarct volumes were determined and neurologic function was assessed by 6-point and 28-point neuroscores. ETB receptor-mediated contraction was studied with myograph and protein expression with immunohistochemistry. In vitro organ culture and tMCAO resulted in vascular ETB receptor upregulation and activation of ERK1/2 that was prevented by U0126. Although no effect on infarct size, U0126 improved the long-term neurologic function after experimental stroke in female rats. In conclusion, early prevention of the ERK1/2 activation and ETB receptor-mediated vasoconstriction in the cerebral vasculature after ischemic stroke in female rats improves the long-term neurologic outcome.

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Liu, Zhao, Mengjie Liu, Gongwei Jia, Jiani Li, Lingchuan Niu, Huiji Zhang, Yunwen Qi, Houchao Sun, Liang-Jun Yan, and Jingxi Ma. "Long-term intermittent fasting improves neurological function by promoting angiogenesis after cerebral ischemia via growth differentiation factor 11 signaling activation." PLOS ONE 18, no. 3 (March 30, 2023): e0282338. http://dx.doi.org/10.1371/journal.pone.0282338.

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Intermittent fasting (IF), an alternative to caloric restriction, is a form of time restricted eating. IF conditioning has been suggested to have neuroprotective effects and potential long-term brain health benefits. But the mechanism underlying remains unclear. The present study focused on the cerebral angiogenesis effect of IF on ischemic rats. Using a rat middle cerebral artery occlusion model, we assessed neurological outcomes and various vascular parameters such as microvessel density (MVD), regional cerebral blood flow (rCBF), proliferation of endothelial cells (ECs), and functional vessels in the peri-infarct area. IF conditioning ameliorated the modified neurological severity score and adhesive removal test, increased MVD, and activated growth differentiation factor 11 (GDF11)/activin-like kinase 5 (ALK5) pathways in a time-dependent manner. In addition, long-term IF conditioning stimulated proliferation of ECs, promoted rCBF, and upregulated the total vessel surface area as well as the number of microvessel branch points through GDF11/ALK5 pathways. These data suggest that long-term IF conditioning improves neurological outcomes after cerebral ischemia, and that this positive effect is mediated partly by angiogenesis in the peri-infarct area and improvement of functional perfusion microvessels in part by activating the GDF11/ALK5 signaling pathway.

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YANPALLEWAR, S., S. RAI, M. KUMAR, and S. ACHARYA. "Evaluation of antioxidant and neuroprotective effect of on transient cerebral ischemia and long-term cerebral hypoperfusion." Pharmacology Biochemistry and Behavior 79, no. 1 (September 2004): 155–64. http://dx.doi.org/10.1016/j.pbb.2004.07.008.

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Kobayashi, Shotai, Shuhei Yamaguchi, Kazunori Okada, Mitsuhiro Kitani, Kazuya Yamashita, Kouichi Shimote, and Tokugoro Tsunematsu. "Effect of Long-Term Administration of Buflomedil on Regional Cerebral Blood Flow in Chronic Cerebral Infarction." Angiology 39, no. 11 (November 1988): 934–41. http://dx.doi.org/10.1177/000331978803901102.

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Razuvaeva, Ya G., E. D. Khaltagarova, A. A. Toropova, K. V. Markova, and D. N. Olennikov. "INFLUENCE OF LOPHANTHUS CHINENSIS DRY EXTRACT ON THE MORPHOFUNCTIONAL STATE OF WISTAR RATS THE BRAIN DURING LONG-TERM ALCOHOLIZATION." Problems of Biological, Medical and Pharmaceutical Chemistry 27, no. 4 (May 9, 2024): 65–71. http://dx.doi.org/10.29296/25877313-2024-05-08.

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The study purpose – to evaluate the effect of the Lophanthus chinensis dry extract on the Wistar rats brain morphofunctional state against the back-ground of long-term alcoholization. Material and methods. Alcohol intoxication was induced by long-term administration (6 weeks) of 40% ethanol in rats. Lophanthus chinensis dry ex-tract at a dose of 100 mg/kg was administered from the 3rd week of the experiment. On days 42-45, the animals were tested in an "open field", an el-evated plus maze, and they developed a conditioned passive avoidance reaction. After which a neurons pathomorphological study in the cerebral cor-tex was carried out. Results. It has been established that L. chinensis dry extract exhibits a neuroprotective effect during long-term alcohol intoxication, preventing the de-velopment of structural disorders in the cerebral cortex, thereby reducing anxiety and emotionality in animals, enhancing orientation-exploratory activity and normalizing mnestic functions. Conclusion. L. chinensis dry extract has a neuroprotective effect during long-term alcohol intoxication.

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Shimizu, Jun, Yasuo Kataama, Hajime Memezawa, Satoru Suzuki, Hiroaki Minamisawa, Shigeru Sugimoto, Toshiyuki Soeda, and Akiro Terashi. "The Effect of the Long-Term Administration of ONO 3144 upon Cerebral Vessels and Experimental Cerebral Ischemia." Japanese Heart Journal 28, no. 4 (1987): 616. http://dx.doi.org/10.1536/ihj.28.616.

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KOBAYASHI, SHOTAI. "Effect of long-term oral administration of buflomedil on local cerebral blood flow in chronic cerebral infarction." Rinsho yakuri/Japanese Journal of Clinical Pharmacology and Therapeutics 19, no. 1 (1988): 287–88. http://dx.doi.org/10.3999/jscpt.19.287.

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Bolbocean, Corneliu, Pia Wintermark, Michael I. Shevell, and Maryam Oskoui. "Perinatal Regionalization and Implications for Long-Term Health Outcomes in Cerebral Palsy." Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques 43, no. 2 (January 21, 2016): 248–53. http://dx.doi.org/10.1017/cjn.2015.322.

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AbstractBackground: Perinatal regionalization is linked to improved neonatal outcomes; however, the effects on long-term outcomes in cerebral palsy (CP) are not known. We estimate the effect of highest levels of neonatal care available at delivery on the risk of developing a nonambulatory CP status. Methods: Children with CP born in Quebec from the Canadian CP Registry excluding postneonatal causes were included (N=360). We estimate the effect of level of care available at delivery on risk of nonambulatory status among children with CP using propensity score matching and instrumental variables methods to adjust for differences in case mix among the three groups of hospitals. The outcome variable is an indicator for CP nonambulation assigned according to Gross Motor Function Classification System (levels IV and V). This study used data that predated therapeutic hypothermia in Quebec. Results: Propensity score estimates of change in the adjusted risk of having a nonambulatory CP status because of birth at level II versus level I is −0.081, 95% confidence interval (CI; −0.2182 to 0.0562); level III versus level I is −0.072 95% CI (−0.225 to 0.08), and level III versus level II is 0.157 95% CI (0.027 to 0.286). Conclusions: Differences in levels of neonatal care available at hospital where the delivery was carried out are not associated with the risk of a nonambulatory CP phenotype. This suggests that level of care and associated medical technology within the Quebec regionalized neonatal-perinatal system is used efficiently because it does not offer any further marginal benefit in the reduction of severe CP outcomes. The system works well as it is, which is supportive of the perinatal regionalization. The success of the neonatal resuscitation program and referral of high-risk births to regional hospitals with sufficient obstetric and perinatal competence and resources may contribute to this lack of variability.

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Chen, Tao, Yuanyuan Zhu, Jia Jia, Han Meng, Chao Xu, Panpan Xian, Zijie Li, Zhengang Tang, Yin Wu, and Yan Liu. "Mitochondrial Transplantation Promotes Remyelination and Long-Term Locomotion Recovery following Cerebral Ischemia." Mediators of Inflammation 2022 (September 15, 2022): 1–8. http://dx.doi.org/10.1155/2022/1346343.

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Cerebral ischemia usually leads to axonal degeneration and demyelination in the adjacent white matter. Promoting remyelination still remains a challenging issue in the field. Considering that ischemia deprives energy supply to neural cells and high metabolic activities are required by oligodendrocyte progenitor cells (OPCs) for myelin formation, we assessed the effects of transplanting exogenous healthy mitochondria on the degenerating process of oligodendrocytes following focal cerebral ischemia in the present study. Our results showed that exogenous mitochondria could efficiently restore the overall mitochondrial function and be effectively internalized by OPCs in the ischemic cortex. In comparison with control cortex, there were significantly less apoptotic and more proliferative OPCs in mitochondria-treated cortex. More importantly, higher levels of myelin basic protein (MBP) and more morphologically normal myelin-wrapped axons were observed in mitochondria-treated cortex at 21 days postinjury, as revealed by light and electron microscope. Behavior assay showed better locomotion recovery in mitochondria-treated mice. Further analysis showed that olig2 and lipid synthesis signaling were significantly increased in mitochondria-treated cortex. In together, our data illustrated an antidegenerating and myelination-promoting effect of exogenous mitochondria, indicating mitochondria transplantation as a potentially valuable treatment for ischemic stroke.

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YOSHIOKA, MITSUHIRO. "Effect of Ibudilast on hippocampal long-term enhanced control by transient cerebral ischemia." Rinsho yakuri/Japanese Journal of Clinical Pharmacology and Therapeutics 29, no. 1/2 (1998): 199–200. http://dx.doi.org/10.3999/jscpt.29.199.

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Rezoagli, E., I. Martinelli, D. Poli, U. Scoditti, S. M. Passamonti, P. Bucciarelli, W. Ageno, and F. Dentali. "The effect of recanalization on long‐term neurological outcome after cerebral venous thrombosis." Journal of Thrombosis and Haemostasis 16, no. 4 (February 8, 2018): 718–24. http://dx.doi.org/10.1111/jth.13954.

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Xin, Bao, Chun-Long Liu, Hong Yang, Cheng Peng, Xiao-Hui Dong, Chuan Zhang, Alex F. Chen, and He-Hui Xie. "Prolonged Fasting Improves Endothelial Progenitor Cell-Mediated Ischemic Angiogenesis in Mice." Cellular Physiology and Biochemistry 40, no. 3-4 (2016): 693–706. http://dx.doi.org/10.1159/000452581.

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Background/Aims: Prolonged fasting (PF) was shown to be of great potency to promote optimal health and reduce the risk of many chronic diseases. This study sought to determine the effect of PF on the endothelial progenitor cell (EPC)-mediated angiogenesis in the ischemic brain and cerebral ischemic injury in mice. Methods: Mice were subjected to PF or periodic PF after cerebral ischemia, and histological analysis and behavioral tests were performed. Mouse EPCs were isolated and examined, and the effects of EPC transplantation on cerebral ischemic injury were investigated in mice. Results: It was found that PF significantly increased the EPC functions and angiogenesis in the ischemic brain, and attenuated the cerebral ischemic injury in mice that was previously subjected to cerebral ischemia. Periodic PF might reduce cortical atrophy and improve long-term neurobehavioral outcomes after cerebral ischemia in mice. The eNOS and MnSOD expression and intracellular NO level were increased, and TSP-2 expression and intracellular O2- level were reduced in EPCs from PF-treated mice compared to control. In addition, transplanted EPCs might home into ischemic brain, and the EPCs from PF-treated mice had a stronger ability to promote angiogenesis in ischemic brain and reduce cerebral ischemic injury compared to the EPCs from control mice. The EPC-conditioned media from PF-treated mice exerted a stronger effect on cerebral ischemic injury reduction compared to that from control mice. Conclusion: Prolonged fasting promoted EPC-mediated ischemic angiogenesis and improved long-term stroke outcomes in mice. It is implied that prolonged fasting might potentially be an option to treat ischemic vascular diseases.

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Fu, Changchang, Yihui Zheng, Kun Lin, Hongzeng Wang, Tingting Chen, Luyao Li, Jiali Huang, et al. "Neuroprotective effect of apigenin against hypoxic-ischemic brain injury in neonatal rats via activation of the PI3K/Akt/Nrf2 signaling pathway." Food & Function 12, no. 5 (2021): 2270–81. http://dx.doi.org/10.1039/d0fo02555k.

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Sasaki, Yasuto, Ayumu Morimoto, Izumi lshii, Shigeru Morita, Masayoshi Tsukahara, and Junichiro Yamamoto. "Preventive Effect of Long-Term Aerobic Exercise on Thrombus Formation in Rat Cerebral Vessels." Pathophysiology of Haemostasis and Thrombosis 25, no. 5 (1995): 212–17. http://dx.doi.org/10.1159/000217163.

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Shapiro, E., W. Krivit, L. Lockman, I. Jambaqué, C. Peters, M. Cowan, R. Harris, et al. "Long-term effect of bone-marrow transplantation for childhood-onset cerebral X-linked adrenoleukodystrophy." Lancet 356, no. 9231 (August 2000): 713–18. http://dx.doi.org/10.1016/s0140-6736(00)02629-5.

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Sakai, Hiroaki, Huaxin Sheng, Robert B. Yates, Kazuyoshi Ishida, Robert D. Pearlstein, and David S. Warner. "Isoflurane Provides Long-term Protection against Focal Cerebral Ischemia in the Rat." Anesthesiology 106, no. 1 (January 1, 2007): 92–99. http://dx.doi.org/10.1097/00000542-200701000-00017.

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Background Long-term neuroprotection by isoflurane has been questioned. The authors examined factors in experimental models potentially critical to definition of enduring isoflurane neuroprotection. Methods Rats were prepared for temporary middle cerebral artery occlusion (MCAO). Pericranial normothermia was maintained. Neurologic deficits (range, 0-48; 0=no deficit) and cerebral infarct volumes were measured. In experiment 1, rats underwent 50 or 80 min MCAO while awake or anesthetized with 1.8% isoflurane. Blood pressure was controlled with phenylephrine. Outcome was evaluated 2 weeks later. In experiment 2, rats underwent 50 min MCAO while awake or anesthetized with isoflurane, with outcome evaluated 8 weeks later. In experiment 3, rats underwent 50 min MCAO while awake or anesthetized with isoflurane and 2 weeks recovery. Effects of phenylephrine and the mitochondrial adenosine triphosphate-sensitive K channel antagonist 5-hydroxydecanoate were studied. In experiment 4, isoflurane-anesthetized rats underwent 50 min MCAO with permanent or temporary common carotid artery occlusion, with outcome evaluated 2 weeks later. Results In experiment 1, isoflurane reduced neurologic deficit (median+/-interquartile range; awake vs. isoflurane: 11+/-12 vs. 8+/-6 for 80 min and 13+/-4 vs. 3+/-9 for 50 min; P=0.0006) and infarct size (160+/-97 vs. 84+/-62 mm for 80 min and 169+/-78 vs. 68+/-61 mm for 50 min; P<0.0001). In experiment 2, isoflurane protection persisted at 8 weeks after ischemia. In experiment 3, there was no effect of phenylephrine or 5-hydroxydecanoate. In experiment 4, permanent common carotid ligation increased infarct size threefold versus temporary occlusion. Conclusions Isoflurane repeatedly improved long-term neurologic and histologic outcome from focal ischemia independent of ischemia duration, perfusion pressure, or pretreatment with 5-hydroxydecanoate.

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Smith, Charity, Jo Contreras-Garza, Rebecca L. Cunningham, Jessica M. Wong, Philip H. Vann, Daniel Metzger, Ella Kasanga, Anthony Oppong-Gyebi, Nathalie Sumien, and Derek A. Schreihofer. "Chronic Testosterone Deprivation Sensitizes the Middle-Aged Rat Brain to Damaging Effects of Testosterone Replacement." Neuroendocrinology 110, no. 11-12 (October 31, 2019): 914–28. http://dx.doi.org/10.1159/000504445.

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Introduction: An increasing number of middle-aged men are being screened for low testosterone levels and the number of prescriptions for various forms of testosterone replacement therapy (TRT) has increased dramatically over the last 10 years. However, the safety of TRT has come into question with some studies suggesting increased morbidity and mortality. Objective: Because the benefits of estrogen replacement in postmenopausal women and ovariectomized rodents are lost if there is an extended delay between estrogen loss and replacement, we hypothesized that TRT may also be sensitive to delayed replacement. Methods: We compared the effects of testosterone replacement after short-term (2 weeks) and long-term testosterone deprivation (LTTD; 10 weeks) in middle-aged male rats on cerebral ischemia, oxidative stress, and cognitive function. We hypothesized that LTTD would increase oxidative stress levels and abrogate the beneficial effects of TRT. Results: Hypogonadism itself and TRT after short-term castration did not affect stroke outcome compared to intact rats. However, after long-term hypogonadism in middle-aged male Fischer 344 rats, TRT exacerbated the detrimental behavioral effects of experimental focal cerebral ischemia, whereas this detrimental effect was prevented by administration of the free-radical scavenger tempol, suggesting that TRT exacerbates oxidative stress. In contrast, TRT improved cognitive performance in non-stroked rats regardless of the length of hypogonadism. In the Morris water maze, peripheral oxidative stress was highly associated with decreased cognitive ability. Conclusions: Taken together, these data suggest that TRT after long-term hypogonadism can exacerbate functional recovery after focal cerebral ischemia, but in the absence of injury can enhance cognition. Both of these effects are modulated by oxidative stress levels.

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Giannopoulos, Sotirios, Aristeidis H. Katsanos, Georgios Tsivgoulis, and Randolph S. Marshall. "Statins and Cerebral Hemodynamics." Journal of Cerebral Blood Flow & Metabolism 32, no. 11 (August 29, 2012): 1973–76. http://dx.doi.org/10.1038/jcbfm.2012.122.

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HMG-CoA reductase inhibitors (statins) are associated with improved stroke outcome. This observation has been attributed in part to the palliative effect of statins on cerebral hemodynamics and cerebral auto regulation (CA), which are mediated mainly through the upregulation of endothelium nitric oxide synthase (eNOS). Several animal studies indicate that statin pretreatment enhances cerebral blood flow after ischemic stroke, although this finding is not further supported in clinical settings. Cerebral vasomotor reactivity, however, is significantly improved after long-term statin administration in most patients with severe small vessel disease, aneurysmal subarachnoid hemorrhage, or impaired baseline CA.

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Li, Fangfang, Haiping Zhao, Ziping Han, Rongliang Wang, Zhen Tao, Zhibin Fan, Sijia Zhang, Guangwen Li, Zhigang Chen, and Yumin Luo. "Xuesaitong May Protect Against Ischemic Stroke by Modulating Microglial Phenotypes and Inhibiting Neuronal Cell Apoptosis via the STAT3 Signaling Pathway." CNS & Neurological Disorders - Drug Targets 18, no. 2 (March 18, 2019): 115–23. http://dx.doi.org/10.2174/1871527317666181114140340.

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Background: Xuesaitong mainly comprises Panax notoginseng saponins and has shown a promising feature in an acute ischemic stroke model; however, its effect on long-term recovery following stroke, and the related mechanisms, are unknown. Methods: The objective of this study was to investigate the long-term protective effects of xuesaitong against ischemic stroke and its effect on microglial polarization. Experimental cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) for 45 min, and C57BL/6 mice were immediately injected with xuesaitong or vehicle through the caudal vein at the onset of cerebral reperfusion consecutively for 14 days. The animals were randomly divided into three groups: a sham-operated group, vehicle-treated group and xuesaitong-treated group at a dose of 15μg/g. Subsequently, 2,3,5-triphenyltetrazolium chloride staining was used to assess infarct volume, and adhesive removal tests and balance beam tests were used to evaluate neurological deficits at days 1, 3, 7 and 14 following ischemia. Reverse-transcriptase polymerase chain reaction and immunofluorescence staining for M1 markers (CD16, iNOS) and M2 markers (CD206, arginase-1) were performed to characterize phenotypic changes in microglia. Elisa was used to determine the release of pro-inflammatory and anti-inflammatory cytokines. TUNEL staining was conducted to detect neuronal cell apoptosis, and western blots were used to determine the activation of signal transducer and activator of transcription 3 (STAT3). Results: Our results revealed that xuesaitong treatment, compared with vehicle treatment, significantly reduced cerebral infarct volume 1 and 3 days after MCAO and resulted in significant improvements in long-term neurological outcomes. Furthermore, xuesaitong treatment, compared with vehicle treatment, significantly reduced M1 markers and elevated M2 markers 7 and 14 days after MCAO at both the mRNA and protein level in ipsilateral brain tissue. This finding was also accompanied by a reduction in neuronal cell apoptosis and p-STAT3 transcription factor levels in the xuesaitong-treated group compared with the vehicle-treated group. Conclusion: We demonstrated that xuesaitong has long-term neuroprotective effects against ischemic stroke, possibly by promoting the polarization of microglia to an M2 phenotype and by inhibiting neuronal cell death via down-regulation of the STAT3 signaling pathway, providing new evidence that xuesaitong might be a promising therapeutic strategy for ischemic stroke.

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Furuya, Kazuhide, Lidong Zhu, Nobutaka Kawahara, Osamu Abe, and Takaaki Kirino. "Differences in infarct evolution between lipopolysaccharide-induced tolerant and nontolerant conditions to focal cerebral ischemia." Journal of Neurosurgery 103, no. 4 (October 2005): 715–23. http://dx.doi.org/10.3171/jns.2005.103.4.0715.

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Object. Although brain tissue may be protected by previous preconditioning, the temporal evolution of infarcts in such preconditioned brain tissue during focal cerebral ischemia is largely unknown. Therefore, in this study the authors engaged in long-term observation with magnetic resonance (MR) imaging to clarify the difference in lesion evolution between tolerant and nontolerant conditions. Methods. Bacterial lipopolysaccharide (LPS; 0.9 mg/kg) was administered intravenously to induce cross-ischemic tolerance. Focal cerebral ischemia was induced 72 hours later in spontaneously hypertensive rats. Serial brain MR images were obtained 6 hours, 24 hours, 4 days, 7 days, and 14 days after ischemia by using a 7.05-tesla unit. Lesion-reducing effects were evident 6 hours after ischemia in the LPS group. Preconditioning with LPS does not merely delay but prevents ischemic cell death by reducing lesion size. Lesion reduction was a sustained effect noted up to 14 days after ischemia. Reduction of local cerebral blood flow (lCBF) in the periinfarct area was significantly inhibited in the LPS group, which was correlated with endothelial nitric oxide synthase (eNOS) expression. Conclusions. Significant preservation of lCBF in the periinfarct area, which is relevant to sustained upregulation of eNOS, could be a candidate for the long-term inhibiting effect on infarct evolution in the LPS-induced tolerant state.

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Suzuki, Satoru, Yasuo Katayama, Hajime Memezawa, Kenji Inamura, Jun Shimizu, Toshiyuki Soeda, Shigeru Sugimoto, and Akiro Terashi. "Effect of the Long-term Antihypertensive Treatment on Cerebral Ischemia induced by BLCL in SHRSR." Japanese Heart Journal 27, no. 4 (1986): 556. http://dx.doi.org/10.1536/ihj.27.556.

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KIMURA, Itaru, Kayoko KUJIRAI, Kazumasa ANDO, and Hareaki SEKI. "Effect of Long-Term Rehabilitation and Welfare Services on Daily Activities in Cerebral Stroke Patients." Japanese Journal of Rehabilitation Medicine 33, no. 4 (1996): 232–36. http://dx.doi.org/10.2490/jjrm1963.33.232.

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Meesen, R. L. J., K. Cuypers, S. P. Swinnen, and O. Levin. "The effect of afferent training on long-term neuroplastic changes in the human cerebral cortex." Brain Stimulation 1, no. 3 (July 2008): 320–21. http://dx.doi.org/10.1016/j.brs.2008.06.222.

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Meesen, Raf L. J., Koen Cuypers, John C. Rothwell, Stephan P. Swinnen, and Oron Levin. "The effect of long-term TENS on persistent neuroplastic changes in the human cerebral cortex." Human Brain Mapping 32, no. 6 (June 9, 2010): 872–82. http://dx.doi.org/10.1002/hbm.21075.

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Tang, Qiang, Tao Ye, Runyu Liang, Yan Wang, Hongyu Li, Jiyao Zhang, Xingxing Yuan, and Luwen Zhu. "Scalp Acupuncture and Treadmill Training Inhibits Neuronal Apoptosis through Activating cIAP1 in Cerebral Ischemia Rats." Evidence-Based Complementary and Alternative Medicine 2021 (November 12, 2021): 1–15. http://dx.doi.org/10.1155/2021/1418616.

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Stroke is the leading cause of long-term disability in developed countries. Multitudinous evidence suggests that treadmill training treatment is beneficial for balance and stroke rehabilitation; however, the need for stroke therapy remains unmet. In the present study, a cerebral ischemia rat model was established by permanent middle cerebral artery occlusion (pMCAO) to explore the therapeutic effect and mechanism of scalp acupuncture combined with treadmill training on ischemic stroke. Terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling and neuronal nuclear protein (NeuN) double staining and cellular inhibitor of apoptosis protein-1 (cIAP1) and NeuN immunofluorescence double staining were used to detect the short-term and long-term neuroprotective effects of scalp acupuncture combined with treadmill training on pMCAO rats. In addition, the antiapoptotic effect of the combined treatment was evaluated in pMCAO rats transfected with cIAP1 shRNA. Western blotting was used to detect the relative protein expression in the caspase-8/-9/-3 activation pathway downstream of cIAP1 to further clarify its regulatory mechanism. Our results showed that scalp acupuncture combined with treadmill training successfully achieved short-term and long-term functional improvement within 14 days after stroke, significantly inhibited neuronal apoptosis, and upregulated the expression of cIAP1 protein in the ischemic penumbra area of the ischemic brain. However, no significant functional improvement and antiapoptotic effect were found in pMCAO rats transfected with cIAP1 shRNA. Western blotting results showed that the combined therapy markedly inhibited the activation of the caspase-8/-9/-3 pathway. These findings indicate that scalp acupuncture combined with treadmill training therapy may serve as a more effective alternative modality in the treatment of ischemic stroke, playing an antiapoptotic role by upregulating the expression of cIAP1 and inhibiting the activation of the caspase-8/-9/-3 pathway.

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Ni, Yaohui, Kefu Cai, Yujie Hu, Chuan-hui Wang, Yuanyuan Zhang, Hua Huang, Xing Su, and Jin-hua Gu. "The Long-Term Outcome Comparison of Different Time-Delayed Kallikrein Treatments in a Mouse Cerebral Ischemic Model." Stem Cells International 2018 (2018): 1–11. http://dx.doi.org/10.1155/2018/1706982.

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Delayed administration of kallikrein after cerebral infarction can improve neurological function. However, the appropriate kallkrein treatment time after ischemic stroke has not been illuminated. In this study, we compared the long-term outcome among three kallikrein therapeutic regimens starting at different time points following mouse cerebral ischemia. Furthermore, the protective mechanisms involving neurogenesis, angiogenesis, and AKT-GSK3β-VEGF signaling pathway were analyzed. Human tissue kallikrein was injected through the tail vein daily starting at 8 h, 24 h, or 36 h after right middle cerebral artery occlusion (MCAO) until the 28th day. Three therapeutic regimens all protected against neurological dysfunction, but kallikrein treatment starting at 8 h after MCAO had the best efficacy. Additionally, kallikrein treatment at 8 h after MCAO significantly enhanced cell proliferation including neural stem cell and induced differentiation of neural stem cell into mature neuron. Kallikrein treatment starting at 8 h also promoted more angiogenesis than other two treatment regimens, which was associated with AKT-GSK3β-VEGF signaling pathway. Thus, we confirm that three delayed kallikrein treatments provide protection against cerebral infarction and furthermore suggest that kallikrein treatment starting at 8 h had a better effect than that at 24 h and 36 h. These findings provide the experimental data contributing to better clinical application of exogenous kallikrein.

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Park, Jong-Min, Ho-Hyun Seong, Han-Byeol Jin, and Youn-Jung Kim. "The Effect of Long-Term Environmental Enrichment in Chronic Cerebral Hypoperfusion-Induced Memory Impairment in Rats." Biological Research For Nursing 19, no. 3 (December 29, 2016): 278–86. http://dx.doi.org/10.1177/1099800416686179.

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Vascular dementia (VaD) is the second most common cause of dementia. It occurs when the cerebral blood supply is reduced by disarrangement of the circulatory system. Environmental enrichment (EE) has been associated with cognitive improvement, motor function recovery, and anxiety relief with respect to various neurodegenerative diseases and emotional stress models. The purpose of this study was to determine whether long-term EE influenced cognitive impairment in a rat model of chronic hypoperfusion induced by permanent occlusion of bilateral common carotid arteries (BCCAo). The Y-maze and Morris water maze tests were performed to evaluate the rats’ cognitive functions. Also, the protein expression of brain-derived neurotrophic factor (BDNF), phosphorylated cAMP-calcium response element binding protein (pCREB), and vascular endothelial growth factor (VEGF) were confirmed by Western blot. The microvessels and angiogenesis-associated proteins in the hippocampal region were investigated using immunohistochemistry. The VaD + EE group showed significantly better cognitive functions than the VaD group in both the Y-maze and MWM tests. In addition, the VaD + EE group showed significantly increased expression of BDNF, pCREB, and VEGF in the hippocampus compared to the VaD group. Rats in the VaD + EE group also had increased length of microvessels and VEGF expression in the hippocampus. These results suggest that long-term EE exerts neuroprotective effects against cognitive impairment induced by chronic cerebral hypoperfusion through the enhancement of BDNF, pCREB, and VEGF expression and indicate that EE may be a good nursing intervention in vascular dementia patients.

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Daileda, Taylor, Farhaan S. Vahidy, Peng Roc Chen, Hooman Kamel, Conrad W. Liang, Sean I. Savitz, and Sunil A. Sheth. "Long-term retreatment rates of cerebral aneurysms in a population-level cohort." Journal of NeuroInterventional Surgery 11, no. 4 (September 5, 2018): 367–72. http://dx.doi.org/10.1136/neurintsurg-2018-014112.

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BackgroundThe likelihood of retreatment in patients undergoing procedures for cerebral aneurysms (CAs) has an important role in deciding the optimal treatment type. Existing determinations of retreatment rates, particularly for unruptured CAs, may not represent current clinical practice.ObjectiveTo use population-level data to examine a large cohort of patients with treated CAs over a 10-year period to estimate retreatment rates for both ruptured and unruptured CAs and explore the effect of changing treatment practices.MethodsWe used administrative data from all non-federal hospitalizations in California (2005–2011) and Florida (2005–2014) and identified patients with treated CAs. Surgical clipping (SC) and endovascular treatments (ETs) were defined by corresponding procedure codes and an accompanying code for ruptured or unruptured CA. Retreatment was defined as subsequent SC or ET.ResultsAmong 19 482 patients with treated CAs, ET was performed in 12 007 (62%) patients and SC in 7475 (38%). 9279 (48%) patients underwent treatment for unruptured CAs and 10203 (52%) for ruptured. Retreatment after 90 days occurred in 1624 (8.3%) patients (11.2% vs 3.7%, ET vs SC). Retreatment rates for SC were greater in unruptured than in ruptured aneurysms (4.6% vs 3.1%), but the opposite was true for ET (10.6% vs 11.8%). 85% of retreatments were within 2 years of the index treatment. Retreatment was associated with age (OR=0.99, 95% CI 0.98 to 0.99), female sex (OR=1.5, 95% CI 1.3 to 1.7), Hispanic versus white race (OR=0.86, 95% CI 0.75 to 0.98), and ET versus SC (OR=3.25, 95% CI 2.85 to 3.71). The adjusted 2-year retreatment rate decreased from 2005 to 2012 for patients with unruptured CAs treated with ET (11% to 8%).ConclusionsRetreatment rates for CAs treated with ET were greater than those for SC. However, for patients with unruptured CAs treated with ET, we identify a continuous decline in retreatment rate over the past decade.

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Schwartz, Marc S., and R. Michael Scott. "Moyamoya syndrome associated with cocaine abuse." Neurosurgical Focus 5, no. 5 (November 1998): E9. http://dx.doi.org/10.3171/foc.1998.5.5.10.

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The authors report the case of a 30-year-old woman who was a long-term intranasal cocaine abuser and who presented with transient ischemic attacks and multiple cerebral infarctions that were associated with moyamoya syndrome. The authors suggest that, because of its sympathomimetic effects, chronic cocaine use may promote intracranial arterial stenosis, distal ischemia, and subsequent formation of moyamoya-like vessels. The patient has remained clinically stable with no new episodes of stroke 6 years after undergoing “pial synangiosis” (modified encephaloduroarteriosynangiosis) to revascularize both hemispheres. Cocaine abuse may lead to moyamoya syndrome and may represent a chronic effect on the cerebral vasculature.

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Yuan, X. Q., T. L. Smith, D. S. Prough, D. S. De Witt, J. W. Dusseau, C. D. Lynch, J. M. Fulton, and P. M. Hutchins. "Long-term effects of nimodipine on pial microvasculature and systemic circulation in conscious rats." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 5 (May 1, 1990): H1395—H1401. http://dx.doi.org/10.1152/ajpheart.1990.258.5.h1395.

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The chronic cranial window preparation allows repeated measurements of the same pial vessels in unanesthetized rats for several weeks and correlation with 24-h monitoring of hemodynamic variables. Nimodipine (20 mg) or placebo was given via two subcutaneous pellets. Large arterioles dilated 26 and 16%, at hour 1 and days 6-13, respectively (P less than 0.02). There was an increase in number of small arterioles throughout the whole observation period with the maximal increment of 47% (P less than 0.05) at days 6-13. Maximal vasodilation with 10% CO2 indicated that the increase in number of small arterioles after administering nimodipine was not caused by the opening of previously closed vessels. The total length of small arterioles and venules increased 47 and 23% at days 6-13, respectively (P less than 0.001). These increases seem to be caused by the increases in the numbers of vessels, because the average length of the small vessels did not appear to change. This suggests that nimodipine reduces cerebral vascular resistance by causing cerebral microvessel neovascularization. Our data demonstrate that the administration of nimodipine (20 mg) is potent in dilating pial arterioles in the short-term without affecting systemic arterial pressure, and that its long-term effect results in new vessel growth.

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Zhang, Chan, Luming Zhen, Zongping Fang, Liang Yu, Yuanyuan Zhang, Haidong Wei, Junfeng Jia, and Shiquan Wang. "Adiponectin Treatment Attenuates Cerebral Ischemia-Reperfusion Injury through HIF-1α-Mediated Antioxidation in Mice." Oxidative Medicine and Cellular Longevity 2021 (July 14, 2021): 1–16. http://dx.doi.org/10.1155/2021/5531048.

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Adiponectin (ADPN) plays an important role in cerebral ischemia-reperfusion injury. Although previous studies have confirmed that ADPN pretreatment has a protective effect on ischemic stroke, the therapeutic effect of ADPN on ischemic stroke and the underlying mechanism are still unclear. In order to clarify these questions, focal transient cerebral ischemia was induced by middle cerebral artery occlusion (MCAO) in mice and ADPN was administered for three times at 6 h, 24 h, and 48 h after reperfusion. Meanwhile, a virus-delivered HIF-1α siRNA was used before ADPN administration. The infarct volume, neurological score, cellular apoptosis, and oxidative stress were assessed at 72 h after reperfusion. The long-term outcome of mice after stroke was recorded as well. The results indicated that ADPN treatment reduced the infarct volume ( P = 0.032 ), neurological deficits ( P = 0.047 ), cellular apoptosis ( P = 0.041 ), and oxidative responses ( P = 0.031 ) at 72 h after MCAO. Moreover, ADPN increased both the protein level and transcriptional activity of HIF-1α as evidenced by the transcription levels of VEGF ( P = 0.046 ) and EPO ( P = 0.043 ) at 72 h after MCAO. However, knockdown of HIF-1α partially reversed the antioxidant and treatment effect of ADPN after cerebral ischemia. In the observation of long-term outcome after ADPN treatment, it demonstrated that ADPN not only prevented the cerebral atrophy ( P = 0.031 ) and the neurological function decline ( P = 0.048 ), but also promoted angiogenesis ( P = 0.028 ) after stroke. In conclusion, our findings suggest that ADPN is effective in treatment of ischemic stroke which could be attributed to the increased antioxidant capacity regulated by HIF-1α.

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Tan, Terence, Jin W. Tee, and Tiew F. Han. "Cell-mediated allergy to cerebral aneurysm clip causing extensive cerebral edema." Journal of Neurosurgery 121, no. 4 (October 2014): 924–28. http://dx.doi.org/10.3171/2014.6.jns132405.

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The authors report the first case of vasogenic cerebral edema due to a cell-mediated hypersensitivity reaction to a nickel-containing aneurysm clip. The patient initially presented for elective clipping of a right middle cerebral artery aneurysm, and on long-term follow-up she demonstrated relapsing-remitting cerebral edema. Four years post–aneurysm clipping, she underwent an exploratory craniotomy given unsuccessful conservative management of her headaches and imaging evidence of cerebral edema with mass effect. During surgery, gross parenchymal edema and inflammatory nodules were observed. Histopathology was consistent with a cell-mediated (Type IV) hypersensitivity reaction. Concerns regarding nickel allergy are often reported in the cardiac literature. This case highlights the possibility of nickel hypersensitivity when using nickel-containing aneurysm clips, especially in patients with known nickel allergies.

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Chebanyuk, S. V., O. E. Svyrydyuk, O. F. Sydorenko, and M. Yu Mamonova. "Cerebral arteriovenous malformations: features of the functioning of the blood circulation system after endovascular treatment with long-term monitoring." Endovascular Neuroradiology 33, no. 3 (December 31, 2020): 19–28. http://dx.doi.org/10.26683/2304-9359-2020-3(33)-19-28.

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Objective ‒ to determine the features of the functioning of the circulatory system in patients with arteriovenous malformations (AVM) of the brain after endovascular operations with long-term observation.Materials and methods. 479 patients with cerebral AVM were examined and treated, of which 377 (78.7 %) were men and 102 (21.3 %) were women. The average age of patients was (27.5±3.5) years. Patients aged 18‒30 years predominated (75.4 %). A dynamic observation of 347 patients after endovascular treatment after 3, 6, 12 and 24 months and more was carried out. Patients underwent cerebral angiography, computed tomography, magnetic resonance imaging, single-photon emission computed tomography, echocardiography, Doppler cardiography, electrocardiography, duplex scanning of cerebral vessels.Results. The study shows the effect of arteriovenous shunting on cerebral and systemic hemodynamics in general. Switching off AVM from the cerebral blood flow improved cerebral hemodynamics already in the early postoperative period, the changes were more significant after 3‒6 months of observation and in some cases reached values in healthy individuals 2 years after the operation. In 52.8 % of patients with AVM, systemic circulation disorders occurred due to an increase in heart rate, minute and stroke blood volumes, left ventricular ejection fraction with an increase in mechanical load on the heart, which led to changes in systolic contraction and diastolic relaxation of the left ventricle of the heart with the development of heart failure. Switching off the AVM from the cerebral blood flow did not cause significant changes in heart functions in the early postoperative period; positive changes occurred over a long period. Dynamic observation showed a positive restructuring of the functioning of the circulatory system in patients after endovascular exclusion of the malformation.Conclusions. Arteriovenous malformations are hemodynamically active systems that lead to hemodynamic-perfusion changes, both at the local and at the general hemodynamic level. The exclusion of the malformation from the bloodstream contributes to the regression of disorders of cerebral and intracardiac blood flow caused by the anatomical and functional characteristics of the malformation itself and its clinical course.

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Hirt, Lorenz, Andrew M. Fukuda, Kamalakar Ambadipudi, Faisil Rashid, Devin Binder, Alan Verkman, Stephen Ashwal, Andre Obenaus, and Jerome Badaut. "Improved long-term outcome after transient cerebral ischemia in aquaporin-4 knockout mice." Journal of Cerebral Blood Flow & Metabolism 37, no. 1 (July 20, 2016): 277–90. http://dx.doi.org/10.1177/0271678x15623290.

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A hallmark of stroke is water accumulation (edema) resulting from dysregulation of osmotic homeostasis. Brain edema contributes to tissue demise and may lead to increased intracranial pressure and lethal herniation. Currently, there are only limited treatments to prevent edema formation following stroke. Aquaporin 4 (AQP4), a brain water channel, has become a focus of interest for therapeutic approaches targeting edema. At present, there are no pharmacological tools to block AQP4. The role of AQP4 in edema after brain injury remains unclear with conflicting results from studies using AQP4−/− mice and of AQP4 expression following stroke. Here, we studied AQP4 and its role in edema formation by testing AQP4−/− mice in a model of middle cerebral artery occlusion using novel quantitative MRI water content measurements, histology and behavioral changes as outcome measures. Absence of AQP4 was associated with decreased mortality and increased motor recovery 3 to 14 days after stroke. Behavioral improvement was associated with decreased lesion volume, neuronal cell death and neuroinflammation in AQP4−/− compared to wild type mice. Our data suggest that the lack of AQP4 confers an overall beneficial role at long term with improved neuronal survival and reduced neuroinflammation, but without a direct effect on edema formation.

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Mori, Sakan, Seizo Sadoshima, Setsuro Ibayashi, Kozo Iino, and Masatoshi Fujishima. "Effect of Long-Term Antihypertensive Treatment on the Cerebral Blood Flow in Patients with Brain Infarction." Cerebrovascular Diseases 3, no. 3 (1993): 154–59. http://dx.doi.org/10.1159/000108691.

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Yokota, Chiaki, Yasuhiro Hasegawa, Kazuo Minematsu, and Takenori Yamaguchi. "Effect of Acetazolamide Reactivity and Long-term Outcome in Patients With Major Cerebral Artery Occlusive Diseases." Stroke 29, no. 3 (March 1998): 640–44. http://dx.doi.org/10.1161/01.str.29.3.640.

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Goodfriend, Karin, Xue-Cheng Liu, and Kimberley Zvara. "Effect of Long Term Orthotic Intervention on Gross Motor Function in Children with Spastic Cerebral Palsy." PM&R 5 (September 2013): S197. http://dx.doi.org/10.1016/j.pmrj.2013.08.270.

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Yi, Ho-Jun, Dong-Hoon Lee, Bo-Young Hong, Seung-Yoon Song, Yeun-Jie Yoo, Mi-Jeong Yoon, Jae-Hoon Sung, and Seong-Hoon Lim. "The Long-Term Functional Effect of Thrombectomy on Patients with Middle Cerebral Artery Occlusion Who Exhibit Moderate to Severe Disability." Medicina 57, no. 5 (May 19, 2021): 509. http://dx.doi.org/10.3390/medicina57050509.

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Background and Objectives: Endovascular thrombectomy (EVT is an emerging gold standard treatment for acute cerebral infarction and may allow functional improvement after subacute cerebral infarction. However, the long-term functional benefits of EVT in patients with moderate to severe disability remain unclear. We investigated the effects of EVT on the activities of daily living (ADL), handicap, gait, and eating in patients with middle cerebral artery (MCA) occlusion who exhibited moderate to severe disability (score of 3–5 on the modified Rankin scale (mRS)) due to stroke, up to six months after onset. Materials and Methods: This retrospective longitudinal case–control study assessed 45 patients with MCA occlusion who exhibited moderate to severe disability (mRS score ≥ 3): 15 underwent EVT and 30 served as controls. Clinical assessments were conducted at two weeks (12–16 days), four weeks (26–30 days), and six months (180–210 days) after stroke onset. Functional assessments comprised the Korean version of the modified Barthel index (MBI), mRS, functional ambulation category (FAC), and dysphagia outcome severity scale (DOSS) to assess disability, handicap, gait, and eating. Results: The MBI, mRS, FAC, and DOSS scores all improved significantly (all p < 0.05) in the EVT group, compared to the controls. Conclusions: EVT has favorable effects on performing routine ADL, the handicap itself, walking, and eating. Therefore, EVT is recommended for patients with acute MCA occlusion, including those with severe disability at the initial assessment.

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Long, Wen, Lubo Zhang, and Lawrence D. Longo. "Fetal and adult cerebral artery KATP and KCa channel responses to long-term hypoxia." Journal of Applied Physiology 92, no. 4 (April 1, 2002): 1692–701. http://dx.doi.org/10.1152/japplphysiol.01110.2001.

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High-altitude long-term hypoxia (LTH) alters cerebral vascular contractile and relaxation responses in both fetus and adult. We tested the hypotheses that LTH-mediated vascular responses were secondary to altered K+ channel function and that in the fetus these responses differ from those of the adult. In middle cerebral arteries (MCA) from both nonpregnant adult and fetal (∼140 days gestation) sheep, which were either acclimatized to high altitude (3,820 m) or sea-level controls, we measured norepinephrine (NE)-induced contractions and intracellular Ca2+ concentration ([Ca2+]i) simultaneously, in the presence or absence of different K+ channel openers or blockers. In adult MCA, LTH was associated with ∼20% decrease in NE-induced tension and [Ca2+]i, with a significant increase in Ca2+ sensitivity. In contrast, in fetal MCA, LTH failed to affect significantly NE-induced contraction or [Ca2+]i but significantly decreased the ATP-sensitive K+ (KATP) channel and Ca2+-activated K+ (KCa) channel-mediated relaxation. The significant effect of KATPand KCa channel activators on the relaxation responses and the fact that K+ channels play a key role in myogenic tone support the hypotheses that K+ channels play an important role in hypoxia-mediated responses. These results also support the hypothesis of significant developmental differences with maturation from fetus to adult.

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Li, Yu-Hui, Dong-Sheng Li, Mei-Qing Wang, Kai Zhao, and Bu-Lang Gao. "Modified hemispherectomy for infantile hemiparesis and epilepsy." Translational Neuroscience 11, no. 1 (October 20, 2020): 380–90. http://dx.doi.org/10.1515/tnsci-2020-0145.

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AbstractObjectiveTo investigate the effect and medical imaging of modified hemispherectomy on patients with infantile hemiparesis and medically refractory epilepsy.Patients and methodsForty-three patients with infantile hemiparesis and refractory epilepsy who underwent hemispherectomy were enrolled. The treatment effect and medical imaging were analyzed.ResultsAnatomical hemispherectomy was successfully performed in all patients (100%). In all patients, the muscular tension decreased and the contracted limbs relaxed. In the pathological examination of the resected brain tissue, secondary cicatricial gyri with concomitant cortical dysplasia was present in 36 cases and polycerebellar gyrus malformation and porencephalia in the other 7 cases. Followed up for 7–15 years (mean 11.3), all patients were alive without a long-term sequela. Epilepsy was satisfactorily controlled, with complete seizure relief in 39 cases (91%) classified as Engel I and basic control in the other 4 (9%) defined as Engel II. The posthemispherectomy medical imaging demonstrated that the intracranial space on the operative side shrank, and the healthy cerebral hemisphere shifted markedly toward the hemispherectomy side, with expanded lateral ventricle on the healthy side and thickened skull and enlarged frontal sinus on the operative side. After 4–5 years, the intracranial space on the operative side disappeared in 75% of the patients, demonstrating enlarged cerebral peduncle on the healthy side.ConclusionFurther modified hemispherectomy in patients with infantile hemiparesis and medically refractory epilepsy demonstrated markedly ameliorated effects on epilepsy control and the prevention of superficial cerebral hemosiderosis in the long-term follow-up.

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Khalil, Mohamed E., Mohamed A. Abdel Ghafar, Osama R. Abdelraouf, Mariam E. Mohamed, Eman M. Harraz, Reem S. Dawood, and Reham A. A. Abouelkheir. "Long-Term Effect of Hyperbaric Oxygen Therapy on Gait and Functional Balance Skills in Cerebral Palsy Children—A Randomized Clinical Trial." Children 10, no. 2 (February 17, 2023): 394. http://dx.doi.org/10.3390/children10020394.

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This study aimed to explore the long-term effects of hyperbaric oxygen therapy on spatiotemporal gait parameters and functional balance in children with cerebral palsy. Thirty-nine children with hemiplegic cerebral palsy were randomly allocated to one of two groups: control or study. The children in both groups received traditional physical therapy three times per week for six months. In addition, the children in the study group received hyperbaric oxygen therapy five times/week for eight weeks. The GAITRite system and pediatric balance scale were used to assess spatiotemporal gait parameters and functional balance at baseline, post-intervention, and six months after the cessation of hyperbaric oxygen therapy. Post-intervention means of all measured parameters were significantly higher than pre-intervention means, but only for the study group (p < 0.05). However, both groups’ means at the six-month follow up were significantly greater than those at pre-intervention (p < 0.05). At the post-intervention and follow-up evaluations, comparisons between groups revealed a statistically significant difference in all measured parameters for the study group against the control group (p < 0.05). It can be concluded that adding hyperbaric oxygen therapy to physical therapy rehabilitation could be effective in improving spatiotemporal gait parameters and functional balance in children with cerebral palsy.

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Stark, Christina, Ibrahim Duran, Kyriakos Martakis, Karoline Spiess, Oliver Semler, and Eckhard Schoenau. "Effect of Long-Term Repeated Interval Rehabilitation on the Gross Motor Function Measure in Children with Cerebral Palsy." Neuropediatrics 51, no. 06 (October 16, 2020): 407–16. http://dx.doi.org/10.1055/s-0040-1715489.

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Abstract Background The efficacy of interventions for cerebral palsy (CP) has been frequently investigated with inconclusive results and motor function measured by the Gross Motor Function Measure (GMFM-66) is common. Objective In this observational analysis, we quantify the GMFM-66 change scores of the second and third year of a multimodal rehabilitation program (interval rehabilitation including home-based, vibration-assisted training) in children with CP. Methods The study was a retrospective analysis of children with CP (2–13 years) participating for a second (n = 262) and third year (n = 86) in the rehabilitation program with GMFM-66 scores at start (M0), after 4 months (M4) of intensive training, and after 8 months of follow-up (M12). A method was previously developed to differentiate between possible treatment effects and expected development under standard of care for GMFM-66 scores using Cohen's d effect size (ES; size of difference). Results After the treatment phase of 4 months (M4) in the second year, 125 of 262 children were responder (ES ≥ 0.2) and 137 children nonresponder (ES < 0.2); mean ES for nonresponder was −0.212 (trivial) and for responder 0.836 (large). After M4 in the third year, 43 children of 86 were responder (ES = 0.881 [large]) and 43 nonresponder (ES = −0.124 [trivial]). Discussion and Conclusion Repeated rehabilitation shows a large additional treatment effect to standard of care in 50% of children which is likely due to the intervention, because in the follow-up period (standard of care), no additional treatment effect was observed and the children followed their expected development.

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Pluta, Ryszard M., John K. B. Afshar, B. Gregory Thompson, Robert J. Boock, Judith Harvey-White, and Edward H. Oldfield. "Increased cerebral blood flow but no reversal or prevention of vasospasm in response to l-arginine infusion after subarachnoid hemorrhage." Journal of Neurosurgery 92, no. 1 (January 2000): 121–26. http://dx.doi.org/10.3171/jns.2000.92.1.0121.

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Object. The reduction in the level of nitric oxide (NO) is a purported mechanism of delayed vasospasm after subarachnoid hemorrhage (SAH). Evidence in support of a causative role for NO includes the disappearance of nitric oxide synthase (NOS) from the adventitia of vessels in spasm, the destruction of NO by hemoglobin released from the clot into the subarachnoid space, and reversal of vasospasm by intracarotid NO. The authors sought to establish whether administration of l-arginine, the substrate of the NO-producing enzyme NOS, would reverse and/or prevent vasospasm in a primate model of SAH.Methods. The study was composed of two sets of experiments: one in which l-arginine was infused over a brief period into the carotid artery of monkeys with vasospasm, and the other in which l-arginine was intravenously infused into monkeys over a longer period of time starting at onset of SAH. In the short-term infusion experiment, the effect of a 3-minute intracarotid infusion of l-arginine (intracarotid concentration 10−6 M) on the degree of vasospasm of the right middle cerebral artery (MCA) and on regional cerebral blood flow (rCBF) was examined in five cynomolgus monkeys. In the long-term infusion experiment, the effect of a 14-day intravenous infusion of saline (control group, five animals) or l-arginine (10−3 M; six animals) on the occurrence and degree of cerebral vasospasm was examined in monkeys. The degree of vasospasm in all experiments was assessed by cerebral arteriography, which was performed preoperatively and on postoperative Days 7 (short and long-term infusion experiments) and 14 (long-term infusion experiment). In the long-term infusion experiment, plasma levels of l-arginine were measured at these times in the monkeys to confirm l-arginine availability.Vasospasm was not affected by the intracarotid infusion of l-arginine (shown by the reduction in the right MCA area on an anteroposterior arteriogram compared with preoperative values). However, intracarotid l-arginine infusion increased rCBF by 21% (p < 0.015; PCO2 38–42 mm Hg) in all vasospastic monkeys compared with rCBF measured during the saline infusions. In the long-term infusion experiment, vasospasm of the right MCA occurred with similar intensity with or without continuous intravenous administration of l-arginine on Day 7 and had resolved by Day 14. The mean plasma l-arginine level increased during infusion from 12.7 ± 4 µg/ml on Day 0 to 21.9 ± 13.1 µg/ml on Day 7 and was 18.5 ± 3.1 µg/ml on Day 14 (p < 0.05).Conclusions. Brief intracarotid and continuous intravenous infusion of l-arginine did not influence the incidence or degree of cerebral vasospasm. After SAH, intracarotid infusion of l-arginine markedly increased rCBF in a primate model of SAH. These findings discourage the use of l-arginine as a treatment for vasospasm after SAH.

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Verkholyak, Dmitry V., Dmitry A. Bakulin, Anatoly K. Brel, and Ivan N. Tyurenkov. "Neuroprotective action of hydroxybenzoic acid derivative with glycine (C40) in the middle cerebral artery occlusion in rats with chronic cerebral circulation insufficiency." Journal of Volgograd State Medical University 20, no. 4 (January 27, 2024): 78–85. http://dx.doi.org/10.19163/1994-9480-2023-20-4-78-85.

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The neuroprotective effect of a novel conjugate of hydroxybenzoic acid with glycine (C40) was investigated in a model of ischemic stroke in rats with chronic cerebral circulation insufficiency (CCCI). The study was conducted in two stages: first, CCCI was modeled by stenosing the common carotid arteries by 50 %, followed by a 60-minute middle cerebral artery occlusion (stroke) after 40 days. Compound C40 and the reference drug citicoline were administered for 10 days before stroke and for 3 days after. Further, neurological deficit (the Garcia and Combs D’Alecy scales), sensorimotor functions (Open Field test, Adhesive Removal test, and Rotarod test), cognitive impairments (Novel Object Recognition and Morris Water Maze tests), cerebral blood flow level, and endothelial function were evaluated. Animals receiving the test substances demonstrated a statistically significant reduction in neurological deficit, less pronounced motor coordination and sensorimotor function impairments, as well as fewer short-term and long-term memory deficits compared to the negative control group. The observed decrease in neurological deficit in the experimental groups was accompanied by improved endothelial function and increased cerebral blood flow. The neuroprotective effect of the novel hydroxybenzoic acid derivative with glycine (C40) was comparable to that of reference drug citicoline.

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Kim, Chi Kyung, Xiu-Li Yang, Young-Ju Kim, In-Young Choi, Han-Gil Jeong, Hong-Kyun Park, Dohoung Kim, et al. "Effect of Long-Term Treatment with Fimasartan on Transient Focal Ischemia in Rat Brain." BioMed Research International 2015 (2015): 1–9. http://dx.doi.org/10.1155/2015/295925.

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Fimasartan is a newly developed angiotensin receptor blocker, which may have protective effects during myocardial infarction or atherosclerosis. In this context, we investigated the effects of long-term treatment with low-dose fimasartan on focal ischemia in rat brain. We induced focal ischemia in brain by transient intraluminal occlusion of middle cerebral artery (MCA) and administered low-dose (0.5 mg/kg) or regular doses (1 or 3 mg/kg) of fimasartan via intravenous routes. After the administration of low-dose (0.5 mg/kg) fimasartan, blood pressure did not decrease compared to the phosphate-buffered saline- (PBS-) control with MCA occlusion (MCAO) group. The infarct volume and ischemic cell death were reduced in the low-dose fimasartan-treated group (46 ± 41 mm3for 0.5 mg/kg and 153 ± 47 mm3for PBS-control with MCAO;P<0.01) but not in the regular-dose groups. Low-dose fimasartan treatment improved functional recovery after ischemia and significantly decreased mortality. In our study, fimasartan reduced the degradation of IκB and the formation of an inflammatory end-product, COX-2. As a result, the recruitment of inflammatory cells in the peri-infarct area decreased in fimasartan-treated group. We have demonstrated that long-term, low-dose fimasartan treatment improved outcomes after focal ischemia in the brain via a reduction of inflammation.

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Niranjan, Ajay, Ahmed Kashkoush, Hideyuki Kano, Edward A. Monaco, John C. Flickinger, and L. Dade Lunsford. "Seizure control after radiosurgery for cerebral arteriovenous malformations: a 25-year experience." Journal of Neurosurgery 131, no. 6 (December 2019): 1763–72. http://dx.doi.org/10.3171/2018.7.jns18304.

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OBJECTIVESeizures are the second-most common presenting symptom in patients with lobar arteriovenous malformations (AVMs). However, few studies have assessed the long-term effect of stereotactic radiosurgery (SRS) on seizure control. The authors of this study assess the outcome of SRS for these patients to identify prognostic factors associated with seizure control.METHODSPatients with AVM who presented with a history of seizure and underwent SRS at the authors’ institution between 1987 and 2012 were retrospectively assessed. The total cohort included 155 patients with a mean follow-up of 86 months (range 6–295 months). Primary outcomes assessed were seizure frequency, antiepileptic drug regimen, and seizure freedom for 6 months prior to last follow-up.RESULTSSeizure-free status was achieved in 108 patients (70%), with an additional 23 patients (15%) reporting improved seizure frequency as compared to their pre-SRS status. The median time to seizure-free status was estimated to be 12 months (95% CI 0–27 months) as evaluated via Kaplan-Meier survival analysis. The mean seizure frequency prior to SRS was 14.2 (95% CI 5.4–23.1) episodes per year. Although not all patients tried, the proportion of patients successfully weaned off all antiepileptic drugs was 18% (28/155 patients). On multivariate logistic regression, focal impaired awareness seizure type (also known as complex partial seizures) and superficial venous drainage were significantly associated with a decreased odds ratio for seizure-free status at last follow-up (OR 0.37 [95% CI 0.15–0.92] for focal impaired awareness seizures; OR 0.36 [95% CI 0.16–0.81] for superficial venous drainage). The effects of superficial venous drainage on seizure outcome were nonsignificant when excluding patients with < 2 years of follow-up. AVM obliteration did not correlate with long-term seizure freedom (p = 0.202, chi-square test).CONCLUSIONSThis study suggests that SRS improves long-term seizure control and increases the likelihood of being medication free, independently of AVM obliteration. Patients with focal impaired awareness seizures were less likely to obtain long-term seizure relief.

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Симанкова, А. А., Е. Н. Сазонова, and О. А. Лебедько. "Effect of neonatal administration of the opioid peptide dalargin on long-term cerebral consequences of antenatal hypoxia." ZHurnal «Patologicheskaia fiziologiia i eksperimental`naia terapiia», no. 3() (September 14, 2018): 31–36. http://dx.doi.org/10.25557/0031-2991.2018.03.31-36.

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Цель исследования - анализ влияния d/m-агониста даларгина (Tyr - D-Ala - Gly - Phe - Leu - Arg) на морфофункциональные показатели головного мозга у половозрелых белых крыс Вистар, перенесших антенатальную гипоксию. Методика. Крысы-самки подвергались воздействию гипобарической гипоксии с 15-х по 19-е сут. гестации. Потомство было разделено на 2 группы: 1) животным группы «Антенатальная гипоксия» (n = 12) интраперитонеально вводили 0,1 мл физиологического раствора с 2-х по 6-е сут. жизни; 2) животным группы «Антенатальная гипоксия + даларгин» (n = 17) в те же сроки интраперитонеально вводили даларгин в дозировке 100 мкг/кг. Группа «Контроль» (n = 25) включала потомство крыс-самок, не подвергавшихся действию гипоксии в период гестации. В гистологических препаратах головного мозга 60-суточных крыс-самцов исследуемых групп определяли площадь ядер и ядрышек нейронов II и V слоев неокортекса и поля СА1 гиппокампа. Активность процессов свободнорадикального окисления в гомогенатах головного мозга определяли методом хемилюминисценции. Поведенческие реакции оценивали в тестах «Открытое поле» и «Приподнятый крестообразный лабиринт». Результаты. У животных группы «Антенатальная гипоксия» выявлено уменьшение массы тела и массы головного мозга; уменьшение числа ядрышек в нейронах II слоя неокортекса и гиппокампа, уменьшение площади ядер нейронов V слоя неокортекса и снижение площади ядрышек нейронов всех исследованных зон; повышение локомоторной активности; активация свободнорадикального окисления в гомогенатах мозга. Введение даларгина уменьшало морфофункциональные церебральные последствия антенатальной гипоксии. Заключение. Показан эффект даларгина для коррекции отдаленных церебральных последствий перенесенной антенатальной гипоксии в эксперименте. The aim of the study was to analyze the effect of d/m-agonist dalargin (Tyr-D-Ala-Gly-Phe-Leu-Arg) on brain morphology and function in mature albino rats exposed to antenatal hypoxia. Methods. Female rats were exposed to hypobaric hypoxia from gestation day 15 to day 19 day. The offspring was divided into 2 groups: 1) the first group, antenatal hypoxia (n = 12), where rats were injected with 0.1 ml of saline from 2 to 6 days of life, 2) the second group, antenatal hypoxia + dalargin (n = 17), where rats were injected with the peptide dalargin (100 mg/kg, i.p.) from 2 to 6 days of life. The control group (n = 25) included offspring of intact female rats. The size of neuronal nuclei and nucleoli in neocortical layers II and V and hippocampal area CA1 were measured on histological slides of the brain from 60-day old male rats. Intensity of free radical oxidation was determined by chemiluminescence in brain homogenates. Rat behavior was evaluated using the open field test and the elevated plus-maze test. Results. Antenatal hypoxia decreased body weight and weight of cerebral hemispheres in 60-day old male albino rats compared with the control. Antenatal hypoxia decreased the number of neuronal nucleoli in layer II of the neocortex and hippocampal area CA1, reduced neuronal nucleus size in layer V of the neocortex and the total area of neuronal nucleoli in all examined brain areas of 60-day-old male albino rats. Animals of this experimental group displayed increased motor activity. The chemiluminescence study of brain homogenates from 60-day-old animals showed increased free radical generation in brain tissues. Administration of dalargin reduced the morphofunctional cerebral consequences of antenatal hypoxia. Conclusion. Dalargin can be used for correcting long-term cerebral consequences of antenatal hypoxia.

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Journal articles on the topic 'Long-Term cerebral effect'

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